What may be relevant in PCOS is that the coexistence of inflammatory signaling via the NF-κB and activator protein 1 (AP-1)/c-Fos/c-Jun pathways results in the activation of serine kinases, I-kappa-B-kinase beta (IKKβ) and c-Jun N-terminal kinase 1 (JNK1), with a subsequent reduction in IRS signaling ability. This evidence concerns the gene JUN and polycystic ovary syndrome.