We subsequently identified additional, chemically diverse molecules that bind to the mutation-induced surface crevice in the Y220C mutant (Basse et al., 2010, Wilcken et al., 2012a) and synthesized a molecule that is biologically active in cancer cell lines with homozygous Y220C mutation (Liu et al., 2013), establishing the proof of concept that functional restoration of mutant p53 by small molecules is a viable strategy. The gene discussed is TP53; the disease is cancer.