Since, on the one hand, nusinersen treatment prevents motor neuron degeneration and consequently formation of astrogliosis and on the other hand, nusinersen treatment might restore SMN protein levels also directly in non‐neuronal tissue such as astrocytes, one could postulate that GFAP concentrations are elevated in the CSF of patients with SMA and decrease in response to nusinersen treatment, proposing cGFAP as a candidate biomarker in SMA. This evidence concerns the gene GFAP and proximal spinal muscular atrophy.