8 March 2023

With nonalcoholic steatohepatitis (NASH) a leading cause of liver disease around the world and numbers expected to rise, emerging understanding of NASH biology and potential new drug targets could not have come at a better time. 

We believe that NASH requires both broad and targeted metabolic and antifibrotic treatment approaches and that precision medicine will help to tackle key genetic drivers of the disease.

For example, a single nucleotide substitution in the PNPLA3 gene severely impairs normal fat breakdown in liver cells. Conversely, in the PSD3 and HSD17B13 genes, a single nucleotide substitution confers a protective effect against NASH. We are investigating how to downregulate PNPLA3 to mimic the protective effects of the mutation in PSD3 and HSD17B13 genes. 

Read more