Table 1(B) further highlights overlapping complement and coagulation proteins, identified for both, longitudinal general population studies with conversion to psychosis and CHR-transition studies, as well as case-control studies (complement: C1Q and C1R; coagulation: FXI and PLG), but also highlights some clear differences that may be a result of distinct study designs or pathophysiological mechanisms during the development of psychosis versus endpoint FEP. This evidence concerns the gene F11 and psychotic disorder.