Spinal Muscular Atrophy (SMA) is a genetic disorder characterized by a spectrum of motor impairments, ranging from infantile onset of severe muscle weakness with respiratory failure to later onset of milder limb weakness and walking impairments (SMA type 3 or 4). While there are pharmaceutical therapies available that can slow the progression of the disease, they do not effectively improve motor deficits, leaving SMA patients significantly impaired. Hence, there is a critical need to develop new combination treatments aimed to improve motor neuron function. Previous experiments conducted in a mouse model have shown that the motor deficit observed in SMA cannot be solely ascribed to spinal motoneurons loss.