In line with these findings, SMA patient fibroblasts treated with lysosomal inhibitors displayed an accumulation of p62, while LC3-II increase was significantly lower than the increase observed in control fibroblasts, suggesting that autophagosome formation was not impaired (Rodriguez-Muela et al., 2018) A potential mechanism that could underlie the autophagic flux defects observed in SMA may be due to the disrupted SNARE complex assembly, an observation that has recently been described following SMN depletion (Kim et al., 2023). This evidence concerns the gene SQSTM1 and proximal spinal muscular atrophy.