One year later, Holzmann et al. reported TRPM4 to be responsible for Ca2+-activated nonselective (CAN) current in PCa, as the large Na+ currents developed upon Ca2+ activation were decreased in PC3, LNCaP, and DU145 PCa cells, as well as primary human prostate epithelial cells (hPEC) with siRNA-based TRPM4 knockdown [41]. Here, TRPM4 is linked to posterior cortical atrophy.