Impacted users can claim credit toward buying future products from Bose, but the decision has still prompted plenty of outcry from SoundTouch owners.
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Over a decade since the range was first introduced, Bose is cutting cloud support for its SoundTouch lineup of wireless smart speakers on February 18, 2026.
Bose customers using speakers from the lineup will lose access to cloud-based integrated music services like Spotify and TuneIn, as well as support for features like multi-room playback. However, they’ll still be able to use their SoundTouch products for audio playback via connected devices using Bluetooth®, AUX, or HDMI, though Bose said it wouldn’t be able to “guarantee long-term performance.” Users also won’t receive any security updates for their SoundTouch speakers after the February cutoff date.
In addition, the SoundTouch app will no longer function after February 18, 2026, though it will still be available for download until February 18, 2026 in markets outside of Japan. Users‘ My Bose accounts will remain active. Recommended by Our Editors
As for why it’s cutting support now, Bose said that technology has evolved since the speakers first launched in 2013 and that it’s “no longer able to sustain the development and support of the cloud infrastructure that powers this older generation of products.”
Though this likely isn’t welcome news for audiophiles who have spent large sums of money on the SoundTouch range—particularly as units such as the SoundTouch 30 retailed for north of $1,000—there is some silver lining. According to Ars Technica, which covered the news, users will be able to claim up to $200 worth of credit from Bose if their devices have been impacted. Head here to enter your serial number and find out if you qualify.
Many Bose users are extremely unhappy about the news. One Reddit user claimed he was now sitting on “$4,000 worth of bricks“ following the move. Meanwhile, others called the ending of support „exploitative“ and even shared links to a petition calling on Bose to renew support for the SoundTouch range, or asked their fellow users to send emails to Bose’s management team.

Naked mole-rats are one of nature’s most extraordinary creatures. These burrowing rodents can live for up to 37 years, around ten times longer than relatives of a similar size. But what is the secret to their extreme longevity? How are they able to delay the decay and decline that befalls other rodents? The answer, at least in part, is due to a switch in a common protein that boosts DNA repair, according to new research published in the journal Science.
Naked mole-rats are one of nature’s most extraordinary creatures. These burrowing rodents can live for up to 37 years, around ten times longer than relatives of a similar size. But what is the secret to their extreme longevity? How are they able to delay the decay and decline that befalls other rodents? The answer, at least in part, is due to a switch in a common protein that boosts DNA repair, according to new research published in the journal Science.
One of the main causes of aging in all animals, including humans, is the accumulation of damaged DNA, our genetic instruction manual. When this damage is not fixed, it leads to defective cells, damaged proteins and eventually a breakdown in the body’s functions.
To understand how the naked mole-rat is so resistant to DNA damage, a study led by researchers at Tongji University in China focused on a common protein called cGAS (cyclic GMP-AMP synthase). In most mammals, cGAS interferes with DNA repair, but the researchers suspected it may have evolved a different function in the long-living rats.
The team compared the cGAS protein in naked mole-rats to that of humans and mice and identified four changes in amino acids (building blocks of cGAS) that flip the protein’s function so that it enhances a cell’s ability to repair damaged DNA.
To test this, the scientists inserted the mole-rat’s unique cGAS into human and mouse cells in the lab. The result was a significant boost in the cells‘ ability to repair their DNA and a reduction in cellular aging. Then, they engineered fruit flies to produce naked mole-rat cGAS and found that they lived around ten days longer than a control group of fruit flies that couldn’t produce cGAS. Finally, they used gene therapy to give the naked mole-rat cGAS to mice. These treated rodents were less frail, had less gray hair and there were fewer old, worn out cells in different organs than mice that didn’t receive the gene.
„This alteration confers naked mole-rat cGAS with a greater capacity to stabilize the genome, counteract cellular senescence and organ aging, and promote extended life span and health span“, commented the researchers.
Research of this nature makes it tempting to wonder if it could be used to increase longevity in humans by modifying amino acids in cGAS. Well, possibly, but there is a long way to go before that could happen. In the meantime, scientists have a new target for developing therapies to treat age-related diseases.
Written for you by our author Paul Arnold, edited by Gaby Clark, and fact-checked and reviewed by Robert Egan—this article is the result of careful human work. We rely on readers like you to keep independent science journalism alive.
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