As this model suggests, obesity-induced pathological changes adipose tissue, such as adipocyte hypertrophy, decreased O2 supply, and increased O2 consumption, lead to the development of adipose tissue hypoxia that, in turn, induces sustained activation of HIF-2α in adipocytes, which then results in both local and systemic inflammation, and contributes to the development of hypertrophic cardiomyopathy. This evidence concerns the gene EPAS1 and hypertrophic cardiomyopathy.