Autophagy is also required for the removal of aberrant stress granules involved in ALS pathology [4] and for downregulation of inflammasome activity, which is activated in response to cellular inclusions formation.[5] TBK1, OPTN, and SQSTM1 converge on autophagy and neuroinflammation, suggesting that compounds which affect both pathways may be promising.[1] A recent paper showed a function for C9orf72 at lysosomes, with impaired responses of mechanistic Target of Rapamycin (mTOR) Complex 1 (mTORC1) signaling to changes in aminoacid availability after depletion of either C9orf72 or SMCR8.[6]. This evidence concerns the gene TBK1 and amyotrophic lateral sclerosis.