Yet, while the increase in LC3B and P62 expression levels in quadriceps muscles (Crippa et al., 2013) or in unseparated hindlimb ALS muscle tissue (Olivan et al., 2015) was interpreted as an enhancement of the autophagic flux in end stage ALS muscles, the impairment of autophagosome formation in live ALS myofibers was interpreted as a suppression of the autophagic pathway (Xiao et al., 2015). The gene discussed is MAP1LC3B; the disease is amyotrophic lateral sclerosis.