Other studies emphasized the role of mitochondrial dysfunction in ALS progression, uncovering complex neuroinflammatory interactions between iPSC-derived astrocytes and microglia, and focusing on alterations in mitochondrial proteins, including voltage-dependent anion channels and components of the respiratory chain, linking energy metabolism defects to neuronal vulnerability.78,79 Lin et al. investigated the contribution of the ALS-associated UBQLN2 P497S mutation in mitochondrial impairment, adding evidence that mitochondrial abnormalities are closely linked to disease pathogenesis in ALS. Here, UBQLN2 is linked to amyotrophic lateral sclerosis.