This suggests that although melanomas rely on increased innate autophagic activity, BRAF-mutated tumors are resistant to further mTOR-dependant stimulation of autophagy and that while combined inhibition of autophagy with chemotherapy might be a viable therapeutic avenue for BRAF wild-type melanomas, targeted therapies that attenuate ER stress may prove a more effective treatment strategy for BRAF mutant melanomas (12, 18, 19). Here, MTOR is linked to melanoma.