In fact, this module appears to play a relevant role in fostering proliferation and survival of transformed breast cells, by mechanisms involving GRK2-mediated HDAC6 activation and the modulation of the acetylation status of a newly identified HDAC6 substrate, the prolyl isomerase Pin1, a fundamental cancer driving node also described to be present in such pathological conditions [177]. Here, GRK2 is linked to cancer.