Notably in the NSC-34 cells rapamycin is able to rescue the effects of the mutation on incorporation of SQSTM1 into phagophores, via currently undefined changes downstream of MTOR-dependent signaling, which must overcome the relatively modest reduction in LC3B-binding activity associated with the mutation; this observation supports the notion that autophagy-enhancing strategies may be beneficial in some cases of ALS. The gene discussed is MAP1LC3B; the disease is amyotrophic lateral sclerosis.