In the context of ALS, oxidative stress, derived from mutant SOD1 leading to high concentrations of reactive oxygen species (ROS), also affects the metabolic functions of mitochondria-ER contact communication leading to changes in well-known pathologies such as endoplasmic reticulum (ER) stress, inflammation, and motor neuron death [22]. Here, SOD1 is linked to amyotrophic lateral sclerosis.