Together, these data indicate that TMPRSS2-ERG overexpression in combination with TP53 inactivation is sufficient to drive prostate tumorigenesis and that DBD mutant p53 (e.g., GOF mutant R172H) can significantly accelerate PCa oncogenesis, confirming a GOF role for the p53 R172H DBD mutation in promoting disease progression and aggressiveness. This evidence concerns the gene TMPRSS2 and posterior cortical atrophy.