A mechanism to reverse multidrug resistance in drug-resistant BC cells is based on the receptor for activated C kinase 1 (RACK1) activity that mediates the binding of Src, a P-gp-binding protein, to the overexpressed P-glycoprotein (P-gp) and modulates the activity of this drug pump, able to efflux anticancer drugs through regulation of the phosphorylation of caveolin-1 (CAV1), a protein that modulates P-gp activity, by Src [74]. This evidence concerns the gene RACK1 and breast cancer.