Because IL-6 and IL-11 are also target genes of active STAT3 and ERK1/2 signaling (32, 48) and Ereg expression can be induced by IL-6 (49), this suggests an intimate crosstalk between IL-6, IL-11, and EREG signaling pathways that, in our model, contributed to increased colitis-associated tumor growth in Phd2-deficient animals. This evidence concerns the gene STAT3 and neoplasm.