Constitutive activation of Stat3 has been known to trigger resistance to apoptosis,29 possibly by upregulation of survivin, IAP1/2, Bcl‐xl and Bcl‐2 expression.30 The results of the FCM and observed protein expression levels from the Western blot assays signified that BBI608 induced apoptosis in ovarian cancer cells in a dose‐dependent manner, as verified by the increase in Bax and cleaved caspase‐3 and the reduction in Bcl‐2 and Mcl‐1. This evidence concerns the gene STAT3 and ovarian cancer.