These data using two different cell models (HCT116 and A375) suggest that both PD-L1 and CD276 are under distinct genetic control pathways (e.g. p53 signaling), with a common pharmacological event being their induction by Nutlin-3 in p53-wt containing cancer cells and elevated PD-L1 upon loss of p53-wt protein function. This evidence concerns the gene CD276 and cancer.