Recent studies have revealed that abnormal DAG content contributed to insulin resistance in different animal models [6,7] due to the activation of conventional protein kinase C (PKC) (α, βI, βII, γ) and novel PKC (δ, ε, η, θ) isoforms that inhibited insulin receptor substrate 1 (IRS1) phosphorylation [8,9]. The gene discussed is PRRT2; the disease is Insulin resistance.