They are linked to tumor cell intrinsic plasticity [30] and in melanoma, they are commonly associated with transcriptional reprogramming and epigenetic changes leading to the activation of alternative survival pathways through upregulation of RTKs such as AXL, PDGFRβ, EGFR or NGFR in a subset of dedifferentiated melanoma cells [3, 7, 14, 17, 31–33]. The gene discussed is PDGFRB; the disease is neoplasm.