These changes were corroborated by measurement of secreted clinical fibrotic markers TIMP-1, pro-collagen 1, YKL-40 and fibronectin, which were all significantly increased in NASH compared to steatotic and control microtissues (Fig. 1c) and the increased expression of genes associated with fibrosis in the NASH microtissues (Fig. 1d and Supp. This evidence concerns the gene TIMP1 and metabolic dysfunction-associated steatohepatitis.