GRK2 and breast carcinoma: For instance, the use of compounds or cellular strategies that impair GRK2 phosphorylation in S670, such as ERK or CDK2 inhibitors, would either hamper or completely impair phosphorylation of HDAC6, and thus, GRK2-dependent effects downstream this deacetylase such as growth factor signaling, proliferation, and anchorage-independent growth of breast cancer cells (Nogues et al., 2016).