MAGOH (mago homolog) is a core component of the exon junction complex (EJC), a ribonucleoprotein complex deposited at exon-exon junctions during pre-mRNA splicing 1. As part of the EJC, MAGOH functions in multiple mRNA metabolism processes, including splicing, nuclear export, translation, and nonsense-mediated decay (NMD) 1. MAGOH forms a tight heterodimer with RBM8A that inhibits EIF4A3 ATPase activity, stabilizing the EJC on spliced mRNAs 2. The MAGOH-RBM8A complex localizes to both the nucleus and centrosome, with centrosomal localization required for proper M-phase progression 3. Beyond core EJC functions, MAGOH regulates alternative splicing of pro-apoptotic genes, including inhibition of Bcl-XS formation [UniProt summary]. Clinically, MAGOH overexpression is associated with poor prognosis across multiple cancers, including gastric cancer, glioma, melanoma, and hepatocellular carcinoma 456. In gastric cancer, MAGOH promotes progression by inhibiting hnRNPA1 expression, thereby facilitating formation of the oncogenic RONΔ160 variant and activating PI3K/AKT signaling 5. Conversely, MAGOH depletion in melanoma induces apoptosis through decreased NMD activity and GADD45A upregulation 7. MAGOH haploinsufficiency causes developmental disorders including microcephaly, establishing its essential role in normal cellular function 1.