The authors postulated that upregulation of CERS1 could be a downstream effect in response to stress in pathogenesis of PD however a recent sphingolipid tracer flux study using dual labelling with 13C16-palmitate showed that C16–C18 ceramides largely originate from the de novo pathway and that this pathway is upregulated when GBA is inhibited by CBE treatment in a macrophage cell model40. The gene discussed is GBA1; the disease is Parkinson disease.