To determine the role of STAT3 inhibition in the anti-CRC effects of AR, HCT-116 and SW480 cells were transiently transfected with an empty vector or a plasmid containing STAT3C, an oncogenic mutant of STAT3 that is constitutively activated without tyrosine phosphorylation (Bromberg et al., 1999). This evidence concerns the gene STAT3 and colorectal carcinoma.