These results indicate that activation of both IKK and JNK by HOCl is required for insulin resistance; secondly, HOCl induces phosphorylation of PKCθ, and suppression of PKCθ attenuates phosphorylation of IKK/JNK and restores insulin-stimulated glucose uptake, implying that PKCθ serves as an upstream kinase of IKK/JNK; thirdly, ONOO− treatment dose dependently induces phosphorylation of PKCθ, whereas an ONOO− scavenger reduces HOCl-stimulated phosphorylation of PKCθ, IKK, JNK, and IRS1-Ser307. This evidence concerns the gene PRRT2 and Insulin resistance.