ALG11 encodes a GDP-mannose-dependent alpha-1,2-mannosyltransferase that catalyzes addition of the fourth and fifth mannose residues to dolichol-linked oligosaccharide precursors on the cytoplasmic face of the endoplasmic reticulum 1. This enzymatic step is essential for synthesizing the Man5GlcNAc2-PP-dolichol core oligosaccharide, which serves as substrate for downstream glycosylation enzymes and ultimately as the glycan donor for protein N-linked glycosylation 1. Mutations in ALG11 cause congenital disorder of glycosylation type 1p (ALG11-CDG), a rare autosomal recessive disorder characterized by hypoglycosylation of serum transferrin and other glycoproteins 2. Clinically, ALG11-CDG presents with severe multisystem involvement, including progressive neurological symptoms such as drug-resistant seizures, developmental delay, microcephaly, hypotonia, and deafness, accompanied by structural brain abnormalities including cerebral atrophy, hypomyelination, and corpus callosum hypoplasia 23. To date, fewer than 20 cases have been documented, though expanded genetic screening continues to identify novel pathogenic variants 4. Emerging therapeutic approaches using liposome-encapsulated mannose-1-phosphate show moderate promise in enhancing glycosylation in ALG11-CDG patient fibroblasts, though less dramatically than in other early-pathway CDG defects 5.