A sequential treatment modality as above may suppress PCa with high VEGFR2 and low miR-221 since sunitinib-treated PC3 prostate cancer cells showed increased miR-221 expression, which is likely an escape response to VEGFR2 inhibition given that sunitinib-mediated cell proliferation blockade was prevented by ectopic overexpression of miR-221 [63]. Here, KDR is linked to prostate carcinoma.