Moreover, according to previous evidence highlighting that the SMA pathophysiology is correlated with altered levels of apoptosis-related proteins (e.g., Bax, Bcl-xL, Bcl2) [12, 27, 33–36], we observed a significant reduction of cells positive to Cleaved Caspase 3 (a pro-apoptotic marker) in moxifloxacin-treated mice compared to VHL pups, confirming the efficacy of the drug in modulating cell death mechanisms. This evidence concerns the gene BCL2L1 and proximal spinal muscular atrophy.