Finally, by unchaining BRAF-mutant melanoma from the stimulatory effects of cancer-associated fibroblasts via the depletion of SEMA6A and its related switched-off pro-survival (PI3K/AKT) and pro-proliferative (MAPK, ΝFκΒ) pathways, the authors were able to rescue the efficiency of BRAF/MEK inhibition against melanoma. The gene discussed is SEMA6A; the disease is melanoma.