We found particularly strong evidence for dysregulation of the complement and coagulation cascade, previously implicated in schizophrenia.46,47,48,49,50 Similar processes have been previously implicated in proteomic studies of the development of PEs in the general population.12,20 Changes in the present CHR study that were consistent with results from these previous PE studies include increases in plasminogen, C1r, clusterin, and complement factor H and decreases in A2M and IGHM. The gene discussed is C1R; the disease is schizophrenia.