IFN-I has been reported to be critical for stimulating stronger immune responses against N67 infection (3, 5, 21, 22), thus, we detected whether SHIP1 deficiency affects the production of IFN-I and found that N67C-infected Ship1-chimeric mice produced significantly higher levels of IFN-α and IFN-β in the serum than the infected WT mice (Fig. 1F and G). The gene discussed is INPP5D; the disease is infection.