Especially in the early stages of the disease, when the tumor microenvironment has not yet formed a highly heterogeneous complex system, it can effectively inhibit the formation of new blood vessels and significantly improve diabetes-related metabolic microenvironmental abnormalities by simultaneously blocking key receptor tyrosine kinases such as VEGFR-2/3, PDGFR-α/β, and FGFR1-3 (45). Here, PDGFRA is linked to diabetes mellitus.