ETFDH and multiple acyl-CoA dehydrogenase deficiency: Based on genotype-phenotype correlation analysis, we suggest that patients with MADD carrying ETFDH splicing, nonsense, or frameshift mutations—which result in complete loss of protein function—might consider undergo timely ultrasound examinations and clinical assessments of liver and kidney function.Many affected individuals with type I (neonatal onset with congenital anomalies) and type II (neonatal onset without congenital anomalies) succumb in the newborn period despite metabolic therapy [9].