Recently, it has become clear that the p53 functional scenario in cancer can also be altered by an unbalanced expression of p53 protein isoforms (i.e., p53α, p53β, p53γ, Δ40p53α, Δ40p53β, Δ40p53γ, Δ133p53α, Δ133p53β, Δ133p53γ, Δ160p53α, Δ160p53β, Δ160p53γ) resulting from a combination of alternative splicing, alternative promoters, and/or alternative translation start sites at the TP53 locus [23]. This evidence concerns the gene TP53 and cancer.