Our key findings include: 1) TRPA1 stimulation elicits NO production and post-translational modifications of Akt at serine 473 and eNOS at serine 1177 (each of which are indicators of protein activation [26,27]), 2) TRPA1-induced increases in CM [Ca2+]i and contractile function occur independently of Akt and eNOS activation and 3) the presence and activation of TRPA1 protects against ischemia-induced cardiomyocyte cell death. This evidence concerns the gene TRPA1 and ischemia.