Based on this, Niu et al. revealed that METTL3 is highly expressed in CUMS rats, and its silencing alleviates cognitive deficits by promoting the m6A-mediated processing and maturation of miR-221-3p through DGCR8, which, in turn, suppresses the expression of GRB2-associated binding protein 1 (Gab1)—a key regulator of synaptic plasticity, inflammation, oxidative stress, and apoptosis in the brain—thereby exacerbating cognitive impairment in CUMS models [107]. The gene discussed is METTL3; the disease is Cognitive impairment.