Indeed, overexpression of the p53LCs not only suppressed the transcriptional activity of exogenous and endogenous wt p53 even in response to cisplatin, nutlin-3, or DOX (Figure 2; Supplementary Figure S3), but also showed significant survival advantage as evidenced by increasing the IC50 of the cancer cells treated with either act D or nultin-3 (Figure 5A‒D; Supplementary Figure S6A‒C). The gene discussed is TP53; the disease is cancer.