These findings suggest that the effect of Dach1 deletion in the prostate is not mediated by coincident loss of RB1. These results are the first to show that endogenous Dach1 restrains features of tumorigenesis in vivo, and are consistent with prior correlative studies showing reduced DACH1 abundance in tumors of the brain, ovary, lung, uterus, non-small cell lung cancer, hepatocellular carcinoma, breast, and prostate cancer [24, 59]. This evidence concerns the gene DACH1 and hepatocellular carcinoma.