For example, JNK has been demonstrated to be an inflammatory kinase involved in the development of obesity related insulin resistance [31]; P38 has been shown to promote gluconeogenesis by direct phosphorylation of PGC-1α, therefore stimulating its transcriptional activity toward gluconeogenic genes [32], [33], [34]; activation of the MEK/ERK pathway can partially inhibit PEPCK expression and is sufficient to mediate the suppression of G6Pase gene expression by phorbol ester [27], [28]. This evidence concerns the gene PPARGC1A and Insulin resistance.