Overexpression of circSTAG1 blocked the translocation of ALKBH5 from the cytoplasm to the nucleus, resulting in the upregulation of m6A modification of the fatty acid amide hydrolase (FAAH) mRNA 3′ UTR and degradation of its stability, which attenuated the astrocyte dysfunction and depressive-like behaviors of CUS mice [66], indicating that nuclear ALKBH5 promotes the progression of depression. This evidence concerns the gene ALKBH5 and major depressive disorder.