IL1B and amyotrophic lateral sclerosis: Moreover, the mutation of these genes indicates the contribution of autophagy (i.e., the intracellular process that allows the sequestering and orderly degradation and recycling of aggregated misfolded proteins and dysfunctional cellular organelles), nuclear factor-kappa B (NF-κB), and the downstream nucleotide-binding domain-like receptor protein 3 (NLRP3) inflammasome (i.e., a multiprotein complex responsible for the activation of inflammatory responses that promotes the maturation and secretion of proinflammatory cytokines interleukin IL-1β and IL-18) to the pathogenesis of ALS [10].