One possibility is that an increase in FLI triggers inflammatory responses, which are later balanced by compensatory anti-inflammatory reactions as FLI surpasses a certain threshold.[36–38] Additionally, inflammation-induced endothelial dysfunction may stabilize through vascular remodeling and adaptive responses.[39] Increased insulin secretion and β-cell compensation might also explain the gradual stabilization of insulin resistance.[40] Further research is necessary to elucidate the mechanisms underlying the nonlinear relationship between FLI and CKM syndrome risk. The gene discussed is INS; the disease is Insulin resistance.