Therefore, we conclude that obatoclax ameliorates ALS phenotypes in mutant FUS iPSC-derived neurons, including reducing cytoplasmic FUS levels, reducing aberrant SG formation, ameliorating defects in protein homeostasis, and reducing degeneration, by inducing autophagy via disruption of BCL2-mediated inhibition of BECN1. The gene discussed is FUS; the disease is amyotrophic lateral sclerosis.