This has led to the development of properdin‐deficient mice, which have been utilized in murine models of asthma,103, 104 arthritis,77, 105, 106 AAA,99, 103 non‐septic107 and septic74 shock, and C3 glomerulopathy.36, 49 These studies have provided key information about the breadth of diseases exacerbated by properdin function and many have been reviewed elsewhere.71, 108, 109 Here, we will focus on the interactions of human properdin with platelets and neutrophils and its potential impact on thromboinflammation in the vasculature. The gene discussed is CFP; the disease is Arthritis.