SQSTM1 and amyotrophic lateral sclerosis: In contrast, ML-SA1, a TRPML1 agonist, was found to induce the release of lysosomal Ca2+ in a dose-dependent manner, thus reducing the accumulation of autophagy-related proteins p62/SQSTM1 and LC3-II, which are elevated by L-BMAA.[91] These findings demonstrate that alterations in [Ca2+]C homeostasis induced by TRPML1 activation can promote autophagy, ultimately rescuing ALS motor neurons.