Given that gene-gene interactions may play a key role in the development of MetS, we hypothesized that SNPs within the aforementioned genes including APOA5, APOC1, BRAP, BUD13, CETP, LIPA, LPL, PLCG1, and ZPR1 may contribute to the etiology of MetS and its individual components independently and/or through complex interactions. The gene discussed is APOC1; the disease is metabolic syndrome.