Given a shared susceptibility to infection caused by complement deficiency in humans and mice and enriched MMcs in the liver, where C3 and other complement components are produced, this hypothesis was investigated by evaluating complement levels and infection susceptibility of C3 NIMA mice (C3–/– mice born to C3+/– mothers) compared with genetically identical C3–/– mice born to complement-deficient mothers, along with C3+/– littermate controls (Figure 1A and Supplemental Figure 1; supplemental material available online with this article; https://doi.org/10.1172/JCI187001DS1). The gene discussed is C3; the disease is complement deficiency.