During the postmyocardial infarction period, we showed that nondiabetic hearts responded with altered levels for transcripts representing markers of inflammation (upregulation of Il10, Tnf, Il1b, and Il6 expressions), apoptosis (upregulation of Tp53, Bax, and caspase 3 expressions), antioxidant defense (downregulation of Gpx3, Gpx4, Gstk1, Txnrd2, Sod3, and catalase expressions), and the prosurvival PI3K/Akt pathway (upregulation of Rps6k, Btk, Pik3cg, and Prkcb and down regulation of pdk2 and Prkcz expressions). The gene discussed is BTK; the disease is infarction.