hypothesized that trametinib‐induced autophagy maybe a mechanism for the secondary resistance to RAF–MEK–ERK inhibitors, and subsequent in vivo experiments confirmed this hypothesis by showing the synergistic antiproliferative effects of MEK1/2 inhibitors combined with chloroquine on patient‐derived xenografts of NRAS‐mutated melanoma [315]. The gene discussed is MAPK1; the disease is melanoma.