These D. melanogaster ALS models, including those based on TBPH mislocalization, C9orf72 repeat expansions, and Sod1 mutations, replicate key pathological features such as dendritic and synaptic defects, dysfunction of nucleocytoplasmic transport, impairment of axonal transport of TDP-43 mRNA granules, and motor and sensory neuron dysfunctions observed in human patients, mouse models, and human stem cell models [70,71,72]. This evidence concerns the gene SOD1 and amyotrophic lateral sclerosis.