Given the synergistic interaction between p38 and p53 in cell-cycle regulation [25], we postulate that, in the absence of p53, p38α could compensate for the loss of the p53 tumor-suppression function; this may explain the augmented UV-induced skin carcinogenesis observed in SB203580-treated p53–/–/SKH mice. Here, TP53 is linked to neoplasm.