To characterize the regulatory mechanism of RB1 in-depth, we performed large-scale genomic analyses of The Cancer Genome Atlas (TCGA) database and found that MYC amplification and RB1 deletion were found to be almost mutually exclusive in multiple cancer types40–42 (Supplementary Fig. 1a), indicating potential cross regulation between the RB1 and MYC pathways. The gene discussed is RB1; the disease is cancer.