Acquired resistance to sunitinib presents itself through the accumulation of the drug in lysosomal vesicles [20], the presence of single nucleotide polymorphisms, the upregulated expression of proangiogenic growth factors, such as angiopoietin, HIF-1α/β, epidermal growth factor receptor (EGFR), fibroblast growth factor (FGF), VEGFR, as well as interleukins (IL-8), the adaptation of the tumor microenvironment [21,22,23], and almost twenty other mechanisms. Here, EGFR is linked to neoplasm.