The outcome of TRPA1 stimulation by oxidative stress may vary depending on the tumor type: for instance, TRPA1-mediated Ca2+ entry engages a non-canonical anti-oxidant defense program in lung and breast cancers [8, 9], while it stimulates mitochondrial dysfunction and apoptosis in glioblastoma multiforme [10, 11]. This evidence concerns the gene TRPA1 and breast cancer.