It was found that LIFR can inhibit GLUT1 expression by activating STAT3, while KRAS mutation reversed this effect, allowing GLUT1 to be consistently expressed and promoting glycolysis (Liu et al., 2021).According to data from The Cancer Genome Atlas (TCGA) and the analysis of 89 informative PDAC tumor samples, KRAS mutation is involved in pancreatic cancer cell aerobic glycolysis (Zhu et al., 2021). Here, LIFR is linked to familial pancreatic carcinoma.