The latest compound (Tomasovic, 2020) specifically blocks ERK1/2 dimer formation and consequent Thr188 phosphorylation (that is a prerequisite for ERK nuclear translocation, oncogenic activation and cardiotoxic side effects (Tomasovic, 2020)), preventing heart failure while preserving ERK1/2 catalytic activity and cytosolic survival signaling. This evidence concerns the gene MAPK3 and heart failure.