Therefore, we investigated in a Caucasian cohort with moderately increased risk of cardiometabolic disease, the associations of these components, especially those of the alternative (i.e., C3, C3a, Bb, FD, FH, and properdin) and classical (i.e., C1q, C1-INH, and C4) pathways with the prevalence of the metabolic syndrome, as well as its incidence during a 7-year follow-up period. The gene discussed is FH; the disease is metabolic syndrome.