Research has demonstrated that AKR1B1 modulates cystine uptake and glutathione synthesis flux in lung cancer cells via the STAT3/SLC7A11 signaling axis.26 Consistently, this study revealed similar patterns in drug-resistant HCC cells, where AKR1B1 knockdown significantly suppressed STAT3 phosphorylation and SLC7A11 protein expression (Fig. 4l). This evidence concerns the gene SLC7A11 and lung cancer.