This further supports the contention that a combination therapy reducing sEH activity with sEH inhibitors which have recently passed phase 1a trials [74], while increasing acylethanolamide tone by either exogenous supplementation or inhibiting their degradation with fatty acid amide hydrolase inhibitors [75], could be a more effective strategy than targeting either pathway independently in treating multifactorial inflammatory diseases like AD [36]. The gene discussed is FAAH; the disease is Alzheimer disease.