Considering our prior data pointing to depressed levels of miR-146a in cortical astrocytes isolated from the mSOD1 mice [20,40]—as well as the potential benefits of its regulation [43], together with its increase in the spinal cord of ALS mice in the symptomatic stage [36]—we selected ALS2, ALS3, ALS6 and ALS7 for the subsequent studies directed at paracrine signaling and miRNA modulation, due to their miR-146a deregulation. This evidence concerns the gene ALS2 and amyotrophic lateral sclerosis.