In addition to the role of sphingosine-1-phosphate in CF, the most significant aspect of CFTR dysfunction, according to the published papers overall, is an imbalance of sphingolipid homeostasis, due to ceramide release from sphingomyelin within the membranes [91] and to a disease-related increase in ceramide synthesis [83, 92]. The gene discussed is CFTR; the disease is cystic fibrosis.