This first study of alternative TrkA splicing in CMM and in BRAF(V600E)-mutated A375 melanoma cells suggests a causal link between reductive stress, UPR activation, alternative TrkA splicing, TrkAIII expression and intracellular activation and metastatic CMM, consistent with a stress-induced, oncogenic, pro-survival role for TrkAIII in CMM progression. The gene discussed is NTRK1; the disease is melanoma.