Indeed, studies have reported i) an increased expression and activity of TRPM8 channel in the plasmalemma of epithelial cells in intracapsular prostate tumors [9], ii) a strong decrease in TRPM8 expression in androgen-dependent extracapsular PCa and in androgen-dependent metastasis [10], iii) an almost complete suppression of TRPM8 expression in prostates of patients treated preoperatively with anti-androgen therapy [11] due to the absolute requirement of Trpm8 gene for a functional androgen receptor (AR) [8, 12]. The gene discussed is TRPM8; the disease is posterior cortical atrophy.