KIT and neoplasm: Most studies have been focusing on potential angiogenic-factor-mediated mechanisms of resistance and the microenvironment of the host [1;9-12;15-17], while relatively little attention has been paid to the contribution of tumor-cell-related mechanisms of resistance to sunitinib, with the exception for sunitinib resistance in c-KIT expressing GIST and acquired resistance to sunitinib by tumor cell expression of the extracellular matrix metalloproteinase inducer [18;19].