Thus, crizotinib and foretinib represent multi-targeted tyrosine kinase inhibitors to block c-Met signaling whereby foretinib was even more efficient to completely abolish both, constitutive and HGF-induced c-Met and subsequent MAP kinase phosphorylation in the ovarian adenocarcinoma as well as in the small cell hypercalcemic ovarian cancer cells. This evidence concerns the gene HGF and ovarian carcinoma.