COG6 (component of oligomeric Golgi complex 6) is a subunit of the conserved oligomeric Golgi (COG) complex essential for maintaining Golgi homeostasis and protein glycosylation. The COG complex regulates intra-Golgi vesicle-mediated transport and retrograde recycling, which are critical for proper presentation of surface glycoproteins including sialic acid receptors 1. COG6 deficiency impairs both N- and O-linked protein glycosylation, resulting in destabilization of Golgi glycosylation machinery 2. Biallelic COG6 variants cause COG6-CDG (congenital disorder of glycosylation type 2L), a severe multisystem disorder characterized by neurological involvement, developmental delay, facial dysmorphism, arthrogryposis, hepatic dysfunction, gastrointestinal abnormalities, and central nervous system malformations including corpus callosum dysgenesis and cerebellar hypoplasia 342. COG6 variants have also been identified in lethal fetal akinesia phenotypes 5. Beyond genetic disease, COG6 variants show epigenetic dysregulation in pulmonary arterial hypertension 6, and a regulatory variant near COG6 is a shared genetic risk locus for rheumatoid arthritis and systemic lupus erythematosus 7. Additionally, COG6 functions as an essential host factor for influenza A virus replication through maintaining proper receptor glycosylation and regulating viral protein degradation 1.