While large-scale genomic landscape studies have revealed frequent genomic alteration occurrences within top cancer-driver genes (e.g., TP53, MYC, PTEN, PI3K/AKT, and RB1)12,13, most somatic mutations arise in tumor suppressor genes (74% TP53, 5.6% PTEN, and 5.6% RB1), further complicating efforts to efficiently target TNBC from a therapeutic perspective. This evidence concerns the gene RB1 and cancer.