This could result in the prevention of cancer lethality and, at the same time, allow pRKIP in the heart to induce a well-tolerated positive inotropy and protect from the development of heart failure in mice; (ii) As EDI preserves cytosolic antiapoptotic and cardio-safe ERK1/2 signaling while suppressing nuclear ERK1/2 signaling, EDI treatment could result in protection from pathological cardiac remodeling and heart failure and the inhibition of cancer cell proliferation. This evidence concerns the gene MAPK3 and cancer.