(A) Normal liver and NASH samples were subjected to immunohistochemistry analysis of CXCL10 and TAZ. Representative images are shown, and quantification of CXCL10+ and TAZ+ area per field was performed. Values represent means ± SEM. **P< 0.01, ***P< 0.001 as indicated. (B) The gene expression profiles in healthy control liver, fatty liver, and NASH patients were obtained from published microarray data (the accession number E-MEXP-3291 [http://www.webcitation.org/5zyojNu7T]). Positive correlation of CXCL10 or TAZ with several proven or potential miR-223 targeted genes and cancer-related genes in NASH patient liver samples. P value is indicated. (C) Gene expression profiles in the livers of normal (n=10) and NASH (n=14) patients were analyzed by RT-qPCR. Positive correlation of miR-223 with cytokine, chemokine, and fibrogenic genes, and proven or potential miR-223 targeted genes and cancer-related gene in NASH patients. P value is indicated. (D) A model depicting the critical role of miR-223 in controlling the progression of NASH. Obesity associated fatty liver upregulates miR-223, which subsequently attenuates many downstream target genes including pro-inflammatory and oncogenic genes, thereby ameliorating NASH progression. In contrast, miR-223 is markedly downregulated in HCC. Such downregulation of miR-223 accelerates HCC progression. Thus, miR-223 is a critical regulator of NASH progression and could be a novel therapeutic target for the treatment of NASH and liver cancer.