This study not only discovered the molecular mechanism underlying the coupling of LPA2-mediated inhibitory signaling to CFTR Cl− channel function at the apical plasma membrane of airway and intestinal epithelial cells (Figure 2), but demonstrated that LPA substantially reduced the CTX-induced intestinal fluid secretion in vivo, which had clinical implications for treating human diseases associated with the hyperactivation of CFTR channel function (e.g., secretory diarrhea). This evidence concerns the gene CFTR and Diarrhea.