Data presented by Toko and collaborators showed that inhibition of ATF6 with 4-(2-aminoethyl) benzenesulfonyl fluoride or knockdown of ATF6 with siRNA decreased cardiac function, increased myocardial infarction mortality rate, and increased cardiomyocyte apoptosis in mice (Toko et al., 2010). The gene discussed is ATF6; the disease is myocardial infarction.