Further, the expression of pathogenic ALS-causing mutations of TDP-43 (A315T), FUS/TLS (R495X), and SOD1-G93A or their respective wild-type variants, or an oxidative stressor or endoplasmic reticulum (ER) stress was sufficient to reduce or inhibit Dicer catalytic activity (Emde et al., 2015). Here, SOD1 is linked to amyotrophic lateral sclerosis.