found that CDK6 amplified in drug‐resistant strains could trigger resistance to abemaciclib and palbocicelli in tumor cells through the induction and binding of the CDK inhibitor protein INK4.[34] Therefore, we implied that the knockdown of IGF2BP2 was accompanied by a decrease in CDK6 protein levels, which presumably increased the drug sensitivity of TNBC cells to CDK4/6 inhibitors. Here, CDK4 is linked to neoplasm.