Our current finding that TMEM16F is functionally coupled to TRPV4 channels raises a provocative question of the molecular identities of Ca2+ sources that activate TMEM16F in viral diseases where TMEM16F plays a significant role in syncytium-formation, namely HIV infection (Zaitseva et al., 2017) and SARS-CoV2-mediated pathological syncytialization (Braga et al., 2021). This evidence concerns the gene ANO6 and viral load.