There are various reasons for the ineffectiveness of imatinib monotherapy in ovarian cancer: downregulation of c-kit and PDGFR may lead to induction of VEGF, inhibition of a single tyrosine kinase might be insufficient to impact downstream signaling cascades, and the molecular targets of imatinib might not be relevant in the occurrence of ovarian cancer in comparison with gastrointestinal stromal tumor or chronic myeloid leukemia where a single specific mutation or a translocation, respectively, can be responsible for the genesis of these two cancers [62]. This evidence concerns the gene PDGFRB and ovarian cancer.