C9orf72 and amyotrophic lateral sclerosis: Allen and colleagues analyzed the basis of the catabolic defect in ALS through an innovative phenotypic metabolic array by profiling fibroblasts and induced neuronal progenitor-derived human induced astrocytes from C9orf72 ALS patients in comparison to controls and evaluating the rates of production of reduced nicotinamide adenine dinucleotides from 91 energy substrates [59].