Furthermore, both endogenous and exogenous Δ40p53 expression significantly suppressed clonogenicity, induced cellular senescence, and upregulated p53 target gene expression in the presence of FL-p53 with or without the TP53 mutation, strongly suggesting that Δ40p53, which lacks the MDM2-interactive TAD-I domain, may exhibit higher tumor suppressor activity than FL-p53. Here, MDM2 is linked to neoplasm.