While the exact pathological mechanism of CCNF mutations in ALS/FTD remains debated, overexpression of the specific ALS/FTD-linked S621G CCNF mutation increased the interaction and led to the aberrant ubiquitylation of the autophagy receptor p62 and resulted in the impairment of autophagosome-lysosome fusion [359]. This evidence concerns the gene SQSTM1 and amyotrophic lateral sclerosis.