Since FOXD3 induction in melanoma cells following RAF inhibitor treatment promotes adaptive resistance by upregulating ERBB3 and activating the NRG1/ERBB3/AKT signaling13, we hypothesized that depletion of SOX10, the upstream regulator of FOXD3, would block the FOXD3/ERBB3/AKT axis and sensitize melanoma cells to the RAF inhibitors. The gene discussed is FOXD3; the disease is melanoma.