We therefore aimed to knock out the function of the tumor suppressor Rb1 using CRISPR-Cas9, because TP53 and RB1 mutations have a tendency to be concurrent in human melanoma patients, as seen in the cBIOPortal (P=0.017) (Berger et al., 2012; Cerami et al., 2012; Gao et al., 2013; Hodis et al., 2012; Hugo et al., 2016; Krauthammer et al., 2012). The gene discussed is TP53; the disease is melanoma.