Two new mouse studies have contributed to our knowledge of the physiological role of miR-122, the most abundant liver microRNA. Tsai et al. found steatohepatitis, fibrosis and HCC-like tumours developed as a result of Mir122a deletion and that re-expression of mir-122a reduced both disease manifestation and tumour incidence. Similarly, Hsu et al. found that Mir122 deletion resulted in hepatosteatosis, hepatitis and the development of HCC-like tumours and that tumorigenesis was inhibited by miR-122 given to a mouse model of HCC.