Another study related to androgen deprivation therapy and development of resistant in PCa suggests that the underlying mechanism involves a constitutively activated intrinsic inflammatory signaling circuit composed of IκBα/NF-κB(p65), miR-196b-3p, Meis2, and PPP3CC, which regulate stemness-associated transcription factors that trigger the enhanced tumorigenicity of CRPC cells, and that interruption or knockdown of any molecule of IκBα/NF-κB(p65), miR-196b-3p, Meis2, and PPP3CC signaling circuits inhibits castration-resistant prostate cancer (CRPC) development [101]. This evidence concerns the gene NFKB1 and posterior cortical atrophy.