For example, there have been limited data examining the role of other components of the endocannabinoid system on depression-pain interactions (2-AG, CB2, peroxisome proliferator-activated receptors, etc.), whether the endocannabinoid modulation of affect and nociception occur through the same or parallel pathways, and the mechanism by which the endocannabinoid system may mediate its effects (neurotransmitters, HPA axis, inflammation, or a combination). This evidence concerns the gene CNR2 and depressive disorder.