The two drugs effectively controlled the tumor growth by blocking the β2-AR, and then consequently suppressing the expression of p-Akt, p-mTOR, Bcl-2, cyclin D1, HK2 and GLUT1, which indicated that propranolol could enhance the efficacy of vemurafenib, a member of TKIs. The gene discussed is SLC2A1; the disease is neoplasm.