Importantly, this study had led also to propose, through analysis of the clonality of genomic events a tumor’s natural history with ERG rearrangements, NKX3-1 deletion, SPOP, and FOXA1 mutations as clonal events, occurring early during the natural history of prostate cancer; these events are followed by genetic alterations at the level of TP53 and CKN1B and, finally, by inactivation of PTEN [72]. This evidence concerns the gene TP53 and prostate cancer.