Our findings, along with our previous study demonstrating AXL/AKT axis-mediated resistance to BRAFi in melanoma with wild-type PTEN26, have uncovered a mechanism by which PTEN status contributes to acquired resistance to BRAFi, and offers a rational strategy to guide clinical testing in pre-identified subsets of patients who relapse during treatment with BRAFi. The gene discussed is AXL; the disease is melanoma.