As expected, the inhibition of MDK by the inhibitor iMDK substantially enhanced the high-dose IFN-γ-induced cell proliferation inhibition and suppressed the low-dose IFN-γ-induced EMT activation and aggressiveness promotion, suggesting that IFN-γ may be used in combination with the MDK inhibitor to improve the therapeutic efficacy and to decrease the pro-tumor adverse effects in OC treatment at the same time. The gene discussed is IFNG; the disease is neoplasm.