WNT3A and WNT/β-catenin pathway downstream effectors were higher expressed in SMA SCOs, in a disease severity manner (Figure 5N), fitting the hypothesis of a dysregulated WNT activity underlying the neuromesodermal misspecification we have detected in SMA and in agreement with the accumulation of β-catenin in an SMA mouse model.91 The gene discussed is SMN1; the disease is proximal spinal muscular atrophy.