Abstract: In the last decade, a new neurological disease concept known as anti-myelin oligodendrocyte glycoprotein antibody (MOG-IgG)-associated disease (MOGAD) has emerged and is currently one of the most focused research areas in the field of neuroimmunology. MOG is a membrane protein mainly expressed on the surface of oligodendrocytes (Zhou et al., 2006). The exact pathogenic role of MOG-IgG in patients with MOGAD remains unclear; however, MOG-IgG has been suggested to cause tissue alterations and damage MOG-expressing cells (Zhou et al., 2006). The pathogenicity of MOG-IgG is further supported by the observation that only a few patients with acquired central nervous system (CNS) demyelinating syndromes exhibit both anti-aquaporin-4 antibody (AQP4-IgG) and MOG-IgG simultaneously, particularly with clear positivity levels of these antibodies as indicated by a cell-based assay result with a titer ≥ 1:100 (Sechi et al., 2021; Banwell et al., 2023). Currently, MOGAD is considered a disease group distinct from multiple sclerosis (MS) or AQP4-IgG-positive neuromyelitis optica spectrum disorder (NMOSD). Compared with patients with AQP4-IgG-positive NMOSD, patients with MOGAD are considered to have a lower relapse rate and milder neurological sequelae. In contrast to patients with AQP4-IgG-positive NMOSD, patients with MOGAD may not necessarily require long-term relapse-prevention treatment unless they show a highly active relapsing clinical course. The benefit of repeated monitoring of serum MOG-IgG titers in patients with MOGAD remains unclear and needs to be evaluated in the future.