One, diagnosed with MADD via prenatal screening, received riboflavin treatment for the first 29 months of their life; however, starting from the age of 3, progressive myopathy was developed, and, at the age of 8, a homozygous nonsense mutation in the MPTb domain of FLAD1 was found, which produced a shortened protein that retained some level of FADS activity [75]. The gene discussed is FLAD1; the disease is multiple acyl-CoA dehydrogenase deficiency.