In the context of PM damage, our prior research has already illuminated the role of TMEM16F in safeguarding PM integrity in response to Ca2+ influx triggered by pore formation in vitro.[30] While it was evident that TMEM16F‐deficient cells succumb to various PM injuries, including those induced by LLO, the in vivo role of TMEM16F during Listeria infection and the underlying molecular mechanisms have remained elusive. Here, ANO6 is linked to listeriosis.