Currently a new therapy aimed at increasing SMN expression raised great expectations (Finkel et al., 2017), even though additional drugs are needed to counteract muscular atrophy: SMN is needed in both neurons and muscles (indeed its requirement is highest when the neuromuscular system is correctly established during development); moreover the efficacy of SMN-based treatments can be poor if the neuromuscular system is compromised, since delayed symptoms can later affect treated patients (Bowerman et al., 2017). This evidence concerns the gene SMN2 and muscular atrophy.