This phenomenon likely involves a p38α/Estrogen Receptor (ER)-dependent signaling mechanism, given that the p38α isoform is hyper-activated in initiated keratinocytes and incipient tumor cells in the absence of p38δ [18], and that p38α has been shown to mediate ER transcriptional activation and signaling to promote cancer cell proliferation and survival [32,33,34,35]. The gene discussed is ESR1; the disease is neoplasm.