While this dual blockade effectively suppresses tumor growth, acquired resistance inevitably arises, prompting exploration of post-progression strategies such as switching CDK4/6 inhibitors (e.g., palbociclib → ribociclib) or altering endocrine partners (e.g., fulvestrant → exemestane) (Schoninger and Blain, 2020; Harbeck et al., 2025). This evidence concerns the gene CDK4 and neoplasm.