In resting cells, observable TK1 activity is low to absent, increasing during G1/S transcription, and peaking at S phase.5 In healthy subjects, levels of TK1 are low to absent, with contrastingly elevated levels observed in patients with a range of malignancies, including breast cancer.6 Notably, the synthesis of TK1 is regulated by the E2F pathway, making it an appealing potential marker for CDK4/6 inhibitors. This evidence concerns the gene TK1 and breast carcinoma.