PLA2G1B deficiency or inactivation gave protection from diet-induced obesity, insulin resistance, hyperglycemia, hyperlipidemia, and atherosclerosis [28–30], and PLA2G1B inhibitors suppressed diet-induced obesity and diabetes effectively in mice [31], implying that PLA2G1B inhibition may be a viable therapeutic option for metabolic diseases. This evidence concerns the gene PLA2G1B and diabetes mellitus.