Loss of function in Rb and TP53 gene3, 28 or gene amplification of N‐MYC29, 30 or Aurora A kinase31, 32 is considered as key genetic predisposition to PCSC associated with elevated SOX2 or BMI1 expression; SOX2 has been shown to upregulate BRN2 and synaptophysin (SYP) leading to NEPC33 and BMI1+SOX2+ cells drive the recurrent PCa.34 This evidence concerns the gene SOX2 and posterior cortical atrophy.