To compare the potential tumorigenic effects of K130M/V131I (Mut) and wild-type (WT) HBx on HCC, the <i>Sleeping Beauty</i> (<i>SB</i>) transposon system was used to deliver HBx Mut and WT into the livers of fumarylacetoacetate hydrolase (<i>Fah</i>)-deficient mice and in the context of <i>transformation related protein 53</i> (<i>Trp53</i>) deficiency.
Since then, NTBC/Nitisone (a drug blocking the pathway upstream of FAH) is successfully used in combination with a diet low in tyrosine and phenylalanine, but patients are still at risk of developing hepatocellular carcinoma.
Tyrosinaemia I (fumarylacetoacetate hydrolase deficiency) is an autosomal recessive inborn error of tyrosine metabolism that produces liver failure in infancy or a more chronic course of liver disease with cirrhosis, often complicated by hepatocellular carcinoma, in childhood or early adolescence.