Although several downstream targets of Y705-phosphorylated STAT3, such as Mcl-1, Survivin and c-Myc, have been known to mediate the role of Y705-phosphorylated STAT3 in tumorigenicity of prostate cancer33, there was no difference in the expression of these mediators between enriched TICs and bulk cancer cells in the current study. This evidence concerns the gene BIRC5 and cancer.