This result serves as proof-of-concept that future development of noncovalent modulators that increase TRiC–Stat3 interactions may be a novel approach to increasing Stat3 activity in the setting of acute injuries such as myocardial infarct [49] or traumatic injury where enhanced Stat3 has been demonstrated to prevent apoptosis of parenchymal cells within critical organs including cardiomyocytes, alveolar epithelial cells, and hepatocytes [50]–[52]. Here, STAT3 is linked to myocardial infarction.