In vitro and in vivo observations for Amyotrophic Lateral Sclerosis (ALS), suggested that mutation of genes associated with the disease (SOD1, TDP-43, FUS, and TAF15), can alter mitochondrial dynamics and induce oxidative stress (Panchal and Tiwari, 2019; Kodavati et al., 2020), coupled to the nuclear accumulation of the nuclear factor erythroid 2-related factor 2 (NRF2), a master regulator of detoxification, AOX, and anti-inflammatory mechanisms (Obrador et al., 2020). Here, TAF15 is linked to amyotrophic lateral sclerosis.