Further investigation proved that YTHDF2 was a downstream target of miR-495, and the upregulated YTHDF2 could inhibit the expression of MOB kinase activator 3 B (MOB3B) by recognizing m6A modification of MOB3B mRNA and inducing mRNA degradation, which consequently promoted tumour tumourigenesis and progression in PCa through an m6A-dependent way. This evidence concerns the gene YTHDF2 and posterior cortical atrophy.