Supporting this concept, our findings clearly demonstrates that Axl inhibition by either R428 or SGI-7079, two differently designed small-molecule TKIs [21, 24], engaged immune effector arms to inhibit tumor progression as evidenced by prominently increased antitumor efficacy in syngeneic mice versus immunodeficient nude mice as well as decreased antitumor efficacy in syngeneic mice depleted of T cells. The gene discussed is AXL; the disease is neoplasm.