This role of RAC1 has been suggested in both treatment resistance and compensatory mechanisms following conventional chemotherapy (in diseases including chronic lymphocytic leukemia and squamous cell carcinoma) as well as targeted therapy (anti-EGFR for lung, anti-HER2/estrogen targeted therapies in breast cancers, BRAF protein inhibitors in melanoma, and anti-angiogenic therapies in prostate cancers). The gene discussed is BRAF; the disease is melanoma.