MCL1 and neoplasm: The tumor resistance to anticancer therapy can be attributed to the participation of STAT3 in antiapoptosis by upregulating antiapoptotic proteins (bcl‐2, Mcl‐1, survivin, etc.; Banerjee and Resat, 2015; Berishaj et al., 2007; Diaz et al., 2006; Gritsko et al., 2006; Hartman et al., 2013) or by activating cell cycle mediators (such as cyclin D1) and many other STAT3‐regulated genes involved in prosurvival signaling and self‐renewal of cancer stem cells (Rajendran et al., 2012; Tan et al., 2014; Yao et al., 2011).