The CDK/cyclin–RB–E2F axis (RB pathway) is frequently deregulated in cancer as a result of mutations or deletions in RB1 (10% in HGSOC), amplification of cyclin genes (CCNE1 is amplified in 20% of HGSOC, CCND1 is amplified in 4%), or functional loss of endogenous CDK inhibitors (CDKi), such as p16INK4A (CDKN2A, downregulated in 30% of HGSOC) (6). This evidence concerns the gene RB1 and cancer.