Testing protein mimetics originally designed to antagonize amyloid formation associated with AD and T2D20,21,23, we identified a cationic tripyridylamide, ADH-6, that effectively abrogates mutant p53 amyloid-like aggregation in human cancer cells, which restores p53’s transcriptional activity, leading to cell cycle arrest and induction of apoptosis. The gene discussed is ADH6; the disease is cancer.