In particular, the observation that the approach used in this work is not efficient in affecting SMN-regulated pathways, including the alternative splicing of genes that are common to FUS-ALS and SMA models and that therefore appear as potential candidates in motor neuron degeneration in both diseases, suggests that the splicing regulation exerted by FUS insists on the same molecular pathway as SMN, and that FUS may act downstream of SMN function and independently from SMN-assisted regulation of snRNP biosynthesis and assembly. The gene discussed is FUS; the disease is proximal spinal muscular atrophy.