Similarly to mice deficient in Mfsd2a, humans with homozygous loss-of-function mutations in Mfsd2a exhibited severe microcephaly and intellectual disability, categorized as primary autosomal microcephaly 15 (23–26), indicating that Mfsd2a-mediated LPC transport is essential for human brain development. The gene discussed is MFSD2A; the disease is Intellectual disability.