In ALS animal models, the overexpression of mutant SOD1 drives microglial activation, autophagy impairment, and hyperexpression of pro-inflammatory factors (e.g., MFG-E8, RAGE, IL-1β, TNF-α, and iNOS), therefore reducing the capacity for mutant SOD1 elimination [149]. The gene discussed is SOD1; the disease is amyotrophic lateral sclerosis.