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Cell organelles, hepatitis C\u2010virus infection, reactive oxygen species produced in mitochondria, and defective insulin signaling due to the arrest of G1 phase to S phase transition of \u03b2\u2010cells have significant roles in the precipitation of the diseases. Adiponectin is anti\u2010inflammatory and anti\u2010atherosclerotic and improves insulin resistance. Low\u2010density lipoprotein (LDL) is atherosclerotic, and LDL\u2010cholesterol in T2DM is associated with high\u2010cardiovascular risk. Further, LDL cholesterol reduction significantly reduces cardiovascular morbidity and mortality. High\u2010density lipoprotein (HDL) is also anti\u2010atherosclerotic due to HDL associated paraoxonase\u20101 serum enzyme, which prevents LDL oxidative modifications and the development of CAD. Moreover, elevated apolipoprotein B and apolipoprotein A\u2010I (ApoB\/ApoA\u2010I) ratio in plasma is also a risk factor for CAD. LDL receptor, adiponectin, and endocannabinoid receptor\u20101 genes are independently associated with CAD and T2DM. Polymorphism of Apo E2 (epsilon2) is a positive factor to increase the T2DM risk and Apo E4 (epsilon4) is a negative factor to reduce the disease risk. Taq 1B polymorphism of cholesterol ester transfer protein (CETP) gene contributes to the development of atherosclerosis, whereas haplotypes of APOA5, APOC3, APOC4, and APOC5 genes are in the same cluster and are independently associated with high plasma triglyceride level, CAD and T2DM. In conclusion, because various genes, LDLR, CETP, APOA5, Apo E, Apo B, and Apo A\u2010I, are associated with the precipitation of CAD associated with T2DM, a personalized diet\u2013gene intervention therapy may be advocated to reduce the disease precipitation. 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