Gene monitoring assays confirmed a negative post-transcriptional regulation of UGT1A9 expression by miR-200a/-183, with low levels of miR-200a/-183 suggesting high levels of UGT1A9, thereby increasing sorafenib β-diglyceride formation in HCC and enhancing drug efficacy (105). Here, UGT1A9 is linked to hepatocellular carcinoma.