RPTOR and amyotrophic lateral sclerosis: Interestingly, although one of the causes of ALS, hexanucleotide repeat expansions in C9orf72, can similarly sequester TFEB within the cytosol (Cunningham et al, 2020) partly through Rag‐GTPase dysregulation (Ji et al, 2020), depletion of another component of ALS pathogenesis, TDP‐43, downregulates RPTOR and thus reduces mTORC1‐mediated phosphorylation of TFEB, promoting its nuclear translocation and transactivation of ATG expression.