Furthermore, a recent study employing mice with the gene-targeted systemic deletion of ATRAP has shown that the development of systemic insulin resistance related to ATRAP deficiency is attributable to the exaggerated adipose tissue inflammation that occurs via the secretion of proinflammatory cytokines and factors derived from enlarged adipocytes, thereby suggesting ATRAP to be a novel molecular target in metabolic disorders in visceral obesity [19]. The gene discussed is AGTRAP; the disease is metabolic disease.