Consistently, in PV mouse models and patients epidermis, enhanced proliferation in concert with increased c-Myc and cyclin D1 have been observed [6,23] and a role of caspase-3 in supporting proliferation in PV is suggested here by the reduction of some of these pro-proliferative mediators in response to caspase-3 inhibitor treatment. The gene discussed is MYC; the disease is acquired polycythemia vera.