CDK2 and neoplasm: Lapatinib-stimulated senescence is linked to elevated levels of p15 and p27 but is not dependent on p16 or p21 expression.[32] Generally, TIS establishes a novel mechanism of action for HER2-targeted drugs and may promote resistance development.[33] INX-315, a specific inhibitor of CDK2, may stimulate cell cycle arrest and senescence in solid malignancies.[34] Therefore, developing senescence-based therapies targeting tumor cells is vital for improving outcomes associated with tumor recurrence.