The overexpression of c-KIT could justify the clinical aggressiveness of melanoma V600K, while the lesser dependence on the ERK/MAPK pathway and the expression of alternative signalling (including PI3K-AKT) may explain why melanoma V600K seems to have a different response to BRAF inhibitor and immunotherapy compared to melanoma V600E [23,24,25]. The gene discussed is BRAF; the disease is melanoma.