Kecskés et al., 2015 reported that TRPM4 activation suppresses angiotensin II-induced cardiac hypertrophy, which is dependent on the activation of the calcineurin-NFAT pathway. It has been proposed that this is due to the Ca2+-dependent modulation of TRPM4 activity, which leads to membrane depolarisation in cardiomyocytes and thus reduces the driving force for Ca2+ influx via store-operated calcium entry (SOCE) through TRP canonical type 1 (TRPC1) and type 3 (TRPC3) ion channels (Kecskés et al., 2015; Wu et al., 2004). Here, TRPM4 is linked to cardiac hypertrophy.