Consistent with the current studies, our findings revealed that constitutively activated STAT3 promoted ovarian cancer cell proliferation, cell invasion, and metastasis, while the inhibition of STAT3 suppressed cell proliferation, cell invasion, and metastasis, most likely through the Slug/Snail-mediated regulation of the EMT markers such as E-cadherin and Vimentin. The gene discussed is STAT3; the disease is ovarian carcinoma.