Type 2 diabetes mellitus (T2DM) is an established risk factor for the development of non-alcoholic steatohepatitis (NASH) and hepatocellular carcinoma (HCC). It leads to an accumulation of advanced glycation end-products (AGEs) in the extracellular matrix of the liver, without altering stiffness. Now, Fan et al. find that AGE-bundled collagen enhances liver viscoelasticity to promote HCC.

To accurately model the cell injury and inflammation in NASH that typically precedes HCC development, human MET with mutant β-catenin was hydrodynamically injected in the tail vein of mice. Transformed foci appeared earlier and grew faster in HiAD-fed mice, and inhibition of AGE production or prevention of AGE–collagen crosslinks slowed tumour growth.