Although Hafezparast et al. demonstrated that the Loa mutation causes axonal transport defect by using an assay for the visualization and quantitation of axonal retrograde transport of motor neuron cultures from Loa/Loa mouse based on a fluorescent fragment of tetanus toxin (TeNT HC), heterozygous knock out of dynein did not exacerbate, but ameliorated, axonal transport in a mutant superoxide dismutase 1 (SOD1) mouse model of ALS [7,12]. This evidence concerns the gene SOD1 and amyotrophic lateral sclerosis.