Clinical and preclinical evidences have suggested that resistance to sunitinib is mediated through cancer cells and tumor microenvironment plasticity to adapt to a VEGFR-independent environment by activating other survival and angiogenic pathways such as PI3K/AKT/mTOR, IL-8 or FGF-2 pathways [21–25]. The gene discussed is MTOR; the disease is neoplasm.