Importantly, such GRK2 upregulation in breast cancer cells would concur with that of HDAC6, known to be overexpressed in these tumor contexts [111, 175, 176], as well as with increased phosphorylation of GRK2 on S670 [111] as a consequence of the hyperactivation of ERK1/2 downstream of hyperactivated EGFR, HER2, estrogen receptors, or alterations in the Ras pathway often found in both luminal and basal breast cancer contexts. This evidence concerns the gene EGFR and breast carcinoma.