However, the excess release of mitochondrial content activates an IFN response, which is detrimental for thermogenic fat development28,31,69,70, increases mitochondrial permeability71, augments inflammasome activation and pyroptosis72, triggers obesity, mitochondrial dysfunction and the mitochondrial pathway of adipocyte apoptosis and may aggravate obesity-associated metabolic diseases29,30,73,74. This evidence concerns the gene IFNA1 and Obesity.