Additionally, a C. elegans model of ALS showed defective autophagy and increased levels of p62; however the removal of p62 alleviated the locomotion defect without restoring the autophagy defects (Baskoylu et al., 2022), suggesting that the autophagy defects are upstream and not dependent on p62 in C. elegans. The gene discussed is SQSTM1; the disease is amyotrophic lateral sclerosis.