AITC (5, 10, 15, and 20 M) induced oxidative stress, as well as the ERK signaling pathway in a human breast carcinoma cell model, which contributed to apoptosis activation (e.g., the upregulation of caspases 3 and 9) and the growth arrest of cells in the G2/M phase (e.g., the increased expression of p21 and the suppression of cyclin B and CDK1), mitochondrial depolarization, and mitochondria-associated protein dysregulation (e.g., reduced Bcl-2 expression and elevated cytochrome c and Apaf1) [255]. The gene discussed is BCL2; the disease is breast carcinoma.