CYP1A1 inhibition by siRNA and proadifen in breast cancer cells [10] or by proadifen in CRC cells [7] reduced the synthesis of 12(S)-HETE and the formation of CCIDs in EC monolayers as well and thus, further supports a role of 12(S)-HETE in the malignancy of CRC. This evidence concerns the gene CYP1A1 and breast carcinoma.