Furthermore, in the mutant SOD1 mouse model, as well as in fALS and sALS patients, miR-155 was found to be elevated and its targeting revealed to restore the dysfunctional microglia and to attenuate disease progression in the ALS mouse model (Koval et al., 2013; Butovsky et al., 2015; Cunha et al., 2018). The gene discussed is SOD1; the disease is amyotrophic lateral sclerosis.