CAT and Insulin resistance: The functioning of these SNPs was explained by their participation in the influx of cells of the immune system into adipose tissue (chemokine receptors), reduced CAT (catalase) expression, and simultaneously increased leptin serum levels (ELF5—E74 like ETS transcription factor 5), or mediated by interferon α/β receptor 2 (IFNAR2) onset of β-cell dysfunction, as well as insulin resistance development via the JAK-STAT pathway [130].