CDK4/6i‐treated cells assumed a flattened and enlarged morphology (Fig EV1J), activated the senescence‐associated‐β‐galactosidase (SA‐β‐gal) (Fig EV1K), and maintained high level of the endogenous CDK4/6i p16 (Fig EV1L), all features that can also be observed in cells treated with other anti‐cancer and senescence‐inducing agents such as the genotoxic drug doxorubicin (Demaria et al, 2017). The gene discussed is CDK4; the disease is cancer.