While IFNα/β and IFNγ are distinct in their receptors, activators and downstream effects, they do experience crosstalk through their mutual regulation of STAT1 phosphorylation, a transcription factor capable of inducing SETDB2, NGFR, p53 and other factors in melanoma dedifferentiation and senescence [37–39]. The gene discussed is IFNA1; the disease is melanoma.