Previous studies have shown that high inducers of uPAR expression in cancer cells such as prostaglandin E2, cadmium, nicotine, lithocholic acid, and lysophosphatidic acid activate uPAR by various molecular pathways [38,39,40,41,42], and Lee et al. demonstrated that IL-1β stimulates the expression of uPAR in gastric cancer [43]. This evidence concerns the gene IL1B and gastric cancer.