Indeed, by genetically knocking-out JNK3 in SMA mice, the authors were able to perform a systemic rescue of the diseased phenotype, resulting in prevented neurodegeneration and death of spinal cord MNs, and in increased skeletal muscle innervation with subsequent reduction of atrophy and improvement of the overall growth Interestingly, the increase in JNK phosphorylation in SMA mice is accompanied by the increase in phospho-c-Jun levels, suggesting that the canonical apoptotic pathway (instead of other JNK-dependent pathways as ATF-2 recruitment) is activated in SMA condition [118]. Here, ATF2 is linked to proximal spinal muscular atrophy.