GRK2 and neoplasm: 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.