In a recent article Morton et al. reported about a new-born female with mitochondrial disorder(MID) due to a mutation in the AIFM1 gene on chromosome Xq26.1 encoding for a mitochondrial matrix protein with oxidoreductase activity involved in electron transport, apoptosis, ferredoxin metabolism, reactive oxygen species generation, and immune system regulation. The patient obviously manifested also in the lungs with follicular bronchiolitis and hypertrophic walls of pulmonary arteries. Overall, this interesting report could be enriched by genetic investigation of the aunt with multiple sclerosis, a more detailed description of the nerve conduction and electromyographic studies, revision of the cerebral MRIs, prospective investigations of clinically unaffected organs, and by excluding autonomic neuropathy