The effectiveness of sorafenib likely stems from its ability to target both cancer cells and cells within the TME, exhibiting inhibitory activity against approximately 40 kinases, predominantly angiogenic receptor tyrosine kinases (RTKs) like vascular endothelial growth factor receptors (VEGFRs) and platelet-derived growth factor receptor-beta (PDGFRβ), as well as drivers of cell proliferation such as RAF1, BRAF, and KIT [14]. Here, PDGFRB is linked to cancer.