Therefore, further functional studies will be necessary to unravel the pathomechanisms underpinning the involvement of miR-10b-5p in SOD1 and TARDBP-ALS neurodegeneration, but worth doing because miR-10b-5p may turn out as a potential therapeutic target, and normalization of expression may have beneficial effects in several pathways including KEAP1-NRF2 stress response associated with neurodegeneration. This evidence concerns the gene TARDBP and amyotrophic lateral sclerosis.