Additional neuroprotective benefits provided by the depletion of SRSF1, which leads to the stimulation of transcripts encoding proteins involved in neuron differentiation, axonogenesis and synaptic transmission (Figure S1C), may explain why the partial suppression of one fly ALYREF gene, which was initially reported as a suppressor of C9ORF72-repeat mediated neurotoxicity in a Drosophila loss-of-function screen [74] and also identified as a binding partner of C9ORF72-repeat RNAs [36, 75], provide poor mitigating effects on the locomotor deficits of C9ORF72-ALS Drosophila [12]. The gene discussed is ALYREF; the disease is amyotrophic lateral sclerosis.