MetS is characterized by caloric excess, insulin resistance, and dyslipidemia, which promote adipocyte hypertrophy, local hypoxia, and HIF-1α–driven low-grade inflammation with TNF-α, IL-6 and MCP-1 signaling, engaging NF-κB/JAK–STAT pathways and worsening insulin resistance (11–13). The gene discussed is HIF1A; the disease is metabolic syndrome.