Although p53 transcriptionally regulates EphA2 expression [49], ERK inhibition causes p53 accumulation in breast cancer cells [50, 51], and high EphA2 levels induced by RNF5 depletion might then promote p53 accumulation by decreasing ERK activation; thus, the reciprocal regulation between p53 accumulation and high EphA2 expression in the context of RNF5 inhibition might amplify p53-related tumor suppression and sensitize tumor cells with wild-type p53 to chemotherapy. This evidence concerns the gene EPHA2 and neoplasm.