Updated publication reference for PubMed record(s): 32703943. FAM50A missense variants are present in Armfield XLID syndrome patients. Zebrafish lacking fam50a display related phenotypes and show dysregulation of the transcriptome, increased spliceosome mRNAs and a preponderance of 3’ alternative splicing events, suggesting a role for Fam50a in the spliceosome C complex. Fam50A protein-protein interaction studies show that in 293T cells FAM50A interacts with spliceosome components. In sum, aberrant mRNA processing caused by FAM50A mutation underpins Armfield XLID syndrome.