A thorough, accurate assessment of the intrahepatic cell populations contributing to Pc/SMO-dependent GLI-mediated signaling and Pc/SMO-independent GLI-mediated signaling in CLD is imperative, due to the therapeutic potential of SMO small molecule inhibitors in the treatment of CLD—currently in stage I clinical trials [13]. The gene discussed is GLI1; the disease is congenital secretory chloride diarrhea 1.