We further explored the role of AQP3 in primary HSCs isolated from patients with non-alcoholic steatohepatitis (NASH), showing an upregulation of its protein and gene expression, which was proportional to the fibrosis stage, by PPARγ through the c-Jun N-terminal kinase (JNK) pathway [83]. Here, PPARG is linked to metabolic dysfunction-associated steatohepatitis.