The expression of AHR target genes was not affected by hypoxia in IL4I1-overexpressing cells, indicating that IL4I1 can also activate aryl hydrocarbon receptor (AHR) in hypoxic (TME).70,71 IL4I1 can improve PD-L1 expression in lung adenocarcinoma through JAK/STAT pathway.72 In addition, IL4I1 overexpression will suppress the function of CTL and enhance T cell exhaustion in colorectal cancer.73 The preclinical evidence supports IL4I1 as a novel target for novel immune checkpoint inhibition. Here, AHR is linked to lung adenocarcinoma.