Pro‐inflammatory cytokines TNFα and IL‐1 accumulate in CKD in serum, as well as in insulin target tissues, where they act on IRS‐1 and PKB/Akt to impede post‐receptor insulin signal transduction.15, 16 In the same tissues, in vitro experiments have demonstrated the capability of TNFα and IL‐1β to upregulate 11β‐HSD1, which in turn also causes insulin resistance through action on IRS‐1 and PKB/Akt.11, 25 Existing biochemical data therefore illustrate a coherent pathway through which inflammation‐mediated upregulation of 11β‐HSD1 leads to insulin resistance. The gene discussed is AKT1; the disease is Insulin resistance.