The hypothesis that C/EBPα p30 possesses functions that are distinct from p42 already emerged over a decade ago, when p30 was found to have the ability to bind to gene promoters and repress gene expression independently of p42 in hepatoma cells.[37] Since then, several groups have provided evidence that p30 is a functional C/EBPα variant that is capable of selectively altering gene expression programs. The gene discussed is CEBPA; the disease is hepatocellular carcinoma.