We propose, therefore, that alternative TrkA splicing, resulting in TrkAIII expression and activation, adds a novel targetable pro-survival oncogenic mechanism to UPR activation [29,30] and low melanoma-inducing transcription factor/anexelecto receptor tyrosine kinase (MITF/Axl) ratios [54] in CMM, which can be blocked by the Trk inhibitors lestaurtinib and entrectinib. Here, NTRK1 is linked to melanoma.