In the absence of androgen, increasing levels of cAMP/PKA pathways have been shown to increase the expression of AR and prostate-specific antigen (PSA) proteins in PC cells [102], which, in turn, can lead to increased androgen signaling, resulting in cell proliferation and subsequent castration-resistant PC (CRPC) [103]. The gene discussed is KLK3; the disease is pachyonychia congenita.