In this context, Tan et al. reported that depletion of endogenous hot-spot R273H, R280K, and R280T mutant p53 isoforms downregulated Akt phosphorylation in MDA-MB-468, MDA-MB-231, and CNE-1 cancer cell lines, respectively, suggesting the involvement of mutant p53 isoforms in the promotion of Akt signaling [108]. The gene discussed is TP53; the disease is cancer.