Wild-type TP53 clearly acts as a negative regulator of cell growth, but considering TP53 mutations solely as LOF mutations would prevent a full understanding of how TP53 mutations drive tumor growth, as TP53 status in human cancer is often defined in binary terms, wild-type versus inactivated, despite accumulating evidence that the majority of mutant p53 proteins are heterogeneous oncogenic proteins with multiple GOF activities and with potential as therapeutic targets. The gene discussed is TP53; the disease is cancer.