IFNA1 and neoplasm: Zhang et al. illustrated IRF5 overexpression in combination with its activating kinase IKKβ reprogramed TAMs to a phenotype that induced anti-tumor immunity and promote tumor regression in OC model.524 In addition, IRF9 was reported to be the critical upstream regulator to mediate growth-inhibitory effects of IFN-α on OC cells, and the anti-tumoral effect of chemerin on OC cells in vitro was regulated by the activation of IFN-α response genes via IRF9.525,526 Therefore, IRF3, IRF5, and IRF9 may be protective and function as anti-tumor factors in OC.