Given the growing recognition of neuromuscular dysfunction as a contributing factor in scoliosis development (Koop, 2009; Krieger et al., 2011; Rummey et al., 2021), and a recent study has shown that variants affecting glycinergic neurotransmission can lead to abnormal spinal neural activity and scoliosis-like phenotypes (Wang et al., 2024), the possibility that GAK may influence curve progression through neural or neuroimmune mechanisms warrants further investigation. The gene discussed is GAK; the disease is scoliosis.