AKR1C3 and hepatocellular carcinoma: Accumulation of LDs was observed in sorafenib-resistant HCC HepG2R and Huh7R cells compared to their parental HCC cells, and supplementation with AKR1C3 inhibitors to suppress the formation of LDs combined with sorafenib in HepG2R and Huh7R cells effectively increased the level of ROS and activated cell apoptosis [133, 137].