Similarly, the discordance between serum TK1 and tumor Ki-67 change in response to palbociclib, as well as, the low serum TK1 activity despite persistent tumor cell proliferation observed in patients in the palbociclib-resistant category, could be explained by the inhibitory effect of palbociclib on CDK4/6 in both cancer and non-cancer cells in this setting of  early-stage disease. The gene discussed is CDK4; the disease is cancer.