To that end, we asked the following questions: (i) if intrinsically disordered mutant p53 does indeed aggregate via an amyloid pathway, can the oligopyridylamide-based α-helix mimetics effectively abolish this process; (ii) if successful, does oligopyridylamide-mediated abrogation of mutant p53 aggregation lead to rescue of p53 function and inhibition of cancer cell proliferation in vitro; and (iii) can this oligopyridylamide-based strategy be applied to reverse tumor growth in vivo without adversely affecting healthy tissue? This evidence concerns the gene TP53 and cancer.