In sum, we demonstrated that Axl inhibition induces antitumor immune responses in two murine tumor models by modulation of CD103+ DC accumulation and activation consequently leading to the priming and activation of adaptive antitumor T cells, which reprograms otherwise immunosuppressive microenvironment into a favorable milieu permitting for synergy with PD-1 blockade to elicit a potent antitumor efficacy. The gene discussed is ITGAE; the disease is neoplasm.