Following tissue inflammation or peripheral nerve injury, CCL2 therefore probably enhances the function of TRPV1 channels and facilitates the nociceptive transmission of DRG nociceptive neurons via two different molecular pathogenic mechanisms: PI3K/Akt-mediated upregulation of TRPV1 mRNA expression, and phospholipase C/protein kinase C-mediated transactivation of TRPV1 channels. Here, AKT1 is linked to peripheral nerve injury.