To determine whether ONOO− was involved in HOCl-induced activation of inflammatory kinases and insulin resistance, 3T3-L1 adipocytes were preincubated with l-NAME (1 mmol/l) to inhibit the production of NO, Cu/Zn SOD (SOD1, 150 U/ml) to remove O2·−, or uric acid (50 μmol/l) to scavenge ONOO− before stimulation with HOCl, and then phosphorylation of PKCθ, IKK, JNK, and IRS1 was evaluated. This evidence concerns the gene IRS1 and Insulin resistance.