Interestingly, sac3 (Fig4) nonsynonymous mutations were also described in approximately 2% of patients with amyotrophic lateral sclerosis (ALS) an incurable motor neuron disease, and in primary lateral sclerosis (PLS) as well.172 In 2014, Colin Martyn and Jun Li provided a comprehensive review on Fig4 deficiency phenotypes and subjacent mechanisms that culminated with the proposal that the deficiency of Fig4 in humans and mice likely corresponds to a new form of LSD.173. This evidence concerns the gene FIG4 and amyotrophic lateral sclerosis.