Faah, short for fatty acid amide hydrolase, is an intracellular enzyme. It is responsible for the hydrolysis of endogenous anandamide (AEA), an endocannabinoid. By terminating the biological effects of AEA, Faah is involved in the endocannabinoid system, which plays a crucial role in maintaining homeostasis, regulating immune response, energy metabolism, cognitive functions, and neuronal activity [1,2]. Gene knockout (KO) and conditional knockout (CKO) mouse models can be valuable for studying Faah's function.

In a murine breast cancer model, high levels of Faah were observed in different breast cancer cell lines. Inhibition of Faah was more effective than exogenous endocannabinoid treatment, and the combination of Faah inhibitors and endocannabinoids was the most effective in inducing apoptosis of breast cancer cells in vitro. In vivo Faah inhibition also reduced breast cancer growth in immunodeficient mice, suggesting Faah inhibition is a promising approach for breast cancer treatment [3]. In rodent models, gene deletion or pharmacological inhibition of Faah prevented stress-induced reductions in AEA and associated increases in basolateral amygdala (BLA) dendritic hypertrophy and anxiety-like behavior. Inhibition of Faah also facilitated long-term fear extinction and rescued deficient fear extinction by enhancing AEA-CB1 receptor signaling and synaptic plasticity in the BLA, indicating Faah's role in stress-related responses [4].

In conclusion, Faah plays essential roles in regulating endocannabinoid levels and is involved in biological processes such as stress response and cancer cell apoptosis. Faah KO and related models have revealed its potential as a therapeutic target in areas like breast cancer treatment and stress-related disorders, contributing to our understanding of these disease mechanisms and potential treatment strategies.