In addition to these well-established functions, a study using high-fat diet (HFD)-fed and NCR1 deficient mice demonstrated that obesity induced the upregulation of NCR1 ligand expression in the VAT, which activates adipose tissue-resident NK cells to rapidly increase IFN-γ production, thereby promoting the accumulation of pro-inflammatory M1 macrophages and insulin resistance [53] (Figure 2). The gene discussed is NCR1; the disease is obesity disorder.