Obesity contributes to AT remodeling and a pro‐inflammatory and insulin‐resistant state, which contributes to ectopic lipid deposition, increased hepatic de novo lipogenesis, excess VAT accumulation, and altered SAT TG turnover (Eissing et al., 2013; Lee et al., 2010; Longo et al., 2019; Nouws et al., 2019). This evidence concerns the gene INS and obesity disorder.