Given the critical role of SALL4 in YAP1-dependent HC-to-CCA malignant reprogramming, we next explored its function in nonmalignant reparative HC-to-CC reprogramming using the validated DDC-fed murine cholestasis model with regenerative HC-to-CC conversion (Fig. 5; refs. 5, 33). This evidence concerns the gene SALL4 and cholestasis.