These mechanisms include the shift in signaling from the epidermal growth factor receptor to the platelet-derived growth factor receptor during progression from non-stem cells to CSCs [9]; epithelial–mesenchymal transition (EMT) associated with PKCα overexpression and activation in two genetic models of breast cancer cells [12]; and activation of erythroblastic leukemia viral oncogene homolog 2 (ErbB2) [13]. This evidence concerns the gene PRKCA and breast carcinoma.