Relevant studies have shown that in hormone receptor-positive (HR+) breast cancer patients, although wild-type p53 deletion does not directly affect CDK4/6i activity or G1 phase arrest, it can promote tumor cells to re-enter the cell cycle and accelerate tumor progression through CDK2-mediated p130 phosphorylation, leading to resistance to CDK4/6 inhibitors (Kudo et al., 2024). Here, CDK2 is linked to neoplasm.