These results might further explain the beneficial effects exerted by miR-125b inhibition in SOD1-G93A microglia and motor neuron survival, thus suggesting that the neuroprotective effect exerted by miR-125b inhibition might depend not only on the suppression of toxic mediators among which IL-1β (Figure 2(a)), TNFα, and NOX2 [19], but also on the direct stimulation of M2 parameters such as IL4R, Arg1, and BDNF in ALS microglia. The gene discussed is TNF; the disease is amyotrophic lateral sclerosis.