SERTAD1 was suggested as a positive regulator of the cell cycle,15,17,29,30 and the potential oncogenic effects of SERTAD1 are suggested by its expression that is upregulated in several types of tumors.29,31–33 SERTAD1 can bind to CDK4 directly and form a quaternary complex with CCND2 and p16 to mediate CDK4 activity.34 Several studies indicated that overexpression of SERTAD1 can provoke hyperproliferation17,30 and inhibition of apoptosis.35 However, a direct link between SERTAD1and cancer pathogenesis remains obscure. The gene discussed is CCND2; the disease is cancer.