Interestingly, over-expression of HES1 increased STAT3 phosphorylation activity in colon cancer cells [49] and the amount of HES1 also correlated with the activity of STAT3 in our rectal cancer cells, indicating a reciprocal feed-forward regulation of STAT3 activity, NOTCH target genes and their products. This evidence concerns the gene HES1 and malignant colon neoplasm.