TP53 and cancer: Once inherited, germline pathogenic variants have a clear preferential expression compared with the non-pathological allele and, importantly, are not affected by the recurrent CDKN2A/B deletions [102,103], suggesting that the two alterations, one in each allele, are both needed to fully disrupt the normal cellular function of P16 and P15, as has been shown for RB1 and TP53 in other cancer models [104].