Comparing the various models, it seems that the timing and/or mechanism of Mst1/Mst2 inactivation influences the ensuing phenotype; deletion early in life in the Alb–Cre model is associated with the most marked oval cell expansion and the highest proportion of mixed HCC/CC histology in the liver tumours, whereas the tumours arising spontaneously in Mst1−/−/Mst2+/− mice, which have little or no oval cell expansion before the random allele loss, are overwhelmingly HCC. Here, MST1 is linked to hepatocellular carcinoma.