It also seems that the β-catenin signaling pathway has a detrimental role in SMA disease progression since its pharmacological inhibition using quercetin, a compound that disrupts the transcriptional activity of the β-catenin-Tcf complex, is able to partially restore motor axon morphology in smn-MO zebrafish larvae, suggesting that quercetin could be a novel therapeutic target for treating SMA at early stages [46]. Here, SMN2 is linked to proximal spinal muscular atrophy.