In addition, upregulation of some transcripts in ALS could reflect compensatory mechanisms preventing axon damage or dysfunction in SOD1G93A axons, including Dhx36 (Bicker et al., 2013), the ALS-causative gene Nek1 (Kenna et al., 2016), F3 (Bizzoca et al., 2009), Rbpms (Hornberg et al., 2013), and Farp1 (Zhuang et al., 2009) (Figure 5E). The gene discussed is DHX36; the disease is amyotrophic lateral sclerosis.