The AXL/TNS2/IRS-1 crosstalk has been shown to influence glucose metabolism in pancreatic cancer cells by upregulating glycolytic enzymes such as Glut4 and PDK1 (Fig. 6).199 In the context of drug resistance, Tian et al. demonstrated that inhibiting AXL enhanced the chemosensitivity of ovarian cancer cells to cisplatin by reducing glycolysis. The gene discussed is AXL; the disease is ovarian carcinoma.