In type 2 diabetes, increased macrophage infiltration into adipose tissue, liver, and muscle contributes to the excessive release of pro-inflammatory cytokines—such as TNF-α, IL-6, and IL-1β—which interfere with insulin signaling by impairing processes such as IRS-1 phosphorylation, ultimately promoting insulin resistance [130,131,132]. The gene discussed is IRS1; the disease is Insulin resistance.