Several studies suggest that MYC is activated through overexpression, amplification, rearrangement, Wnt/β-catenin pathway activation, germline MYC promotor variation, and loss of FOXP3 in PCa [76,77,78,79], and is a critical oncogenic event driving PCa initiation and progression [71,80]. Here, FOXP3 is linked to posterior cortical atrophy.