Along the same lines, overexpression of NF-κB subunit p65 and IκBKβ in single muscles of rats using in vivo electrotransfer had no effect on glucose disposal in muscle under hyperinsulinaemic–euglycaemic clamp conditions, suggesting that activation of the IκBKβ–NF-κB pathway in muscle does not seem to be an important local mediator of insulin resistance [31]. This evidence concerns the gene NFKB1 and Insulin resistance.