Remarkably, LC3B-II was significantly further increased (Figure 5B) while both the monomeric, as well as the oligomeric forms (although this latter not reaching the statistical significance, p = 0.06) of SQSTM1/p62 were decreased in ALS mice by AXX71-treatment (Figure 5C), thus suggesting that the compound was able to partially restore autophagy defects, probably by degrading SQSTM1/p62 protein [38]. Here, SQSTM1 is linked to amyotrophic lateral sclerosis.