found that the miR-17–92 cluster, originating from the extracellular EVs of M2-like macrophages, stimulated the imbalance of TGF-β1/BMP-7 pathways in HCC cells by inducing TGF-β type II receptor (TGFBR2) post-transcriptional silencing and inhibiting activin A receptor type 1 (ACVR1) post-translational ubiquitylation by targeting Smad ubiquitylation regulatory factor 1 (Smurf1), thus improving HCC cell growth and metastasis (58). Here, TGFBR2 is linked to hepatocellular carcinoma.