Further, the rearrangement of MAG12 (PTEN inhibitor), BRAF, RAF, and CADM2, their overexpression and mutations in PIK3CA1, the deletion and downregulation of PHLPP1/2, a point mutation in Akt1, mutations in SPOP, CHD1, MLL2, ASH2L, and MED12, the overexpression of SPINK1, MYC, and NMYC, the elevated expression of EZH2 and BM1, the deletion of TAK1/MAP3K7, and the loss of TP53 also play a role in PCa pathogenesis [23]. This evidence concerns the gene MAP3K7 and posterior cortical atrophy.