On the contrary, the hypo‐phosphorylated Rb1 protein, preventing E2F release, would favour the interaction of E2F repressors (E2F4 and E2F5) on the promoter of survivin, allowing for a gene transcription repression in non‐transformed embryonic fibroblast cells.57 Our data are suggestive for linking hypo‐pRb1 to the negative regulation of survivin protein expression in SK‐H‐SH (N) cells.57 The inhibition of survivin may represent an additional advantage in neoplastic patients, since through this action aspirin might enhance the effect of cytotoxic drugs to cancer cells. The gene discussed is PRB1; the disease is cancer.