While in the cellular models of ALS, mutated FUS seems to hamper the formation of autophagosome, in ALS patients and model organisms with different protein mutations (e.g., SOD1, TDP-43, FUS) the accumulation of autophagosome might also be a consequence of the activation of macroautophagy, chaperone-mediated autophagy, and microautophagy (Codogno et al., 2012; Nassif et al., 2014; Chen et al., 2015; Xiao et al., 2015; Sellier et al., 2016; Kaushik and Cuervo, 2018). The gene discussed is FUS; the disease is amyotrophic lateral sclerosis.