In the current study, we convincingly show that interference with ERKT188-phosphorylation indeed prevents cardiac hypertrophy and maladaptive remodeling, interferes with major hypertrophic signaling pathways19,22,44,45 such as Myc- and NFAT-associated gene regulation in mice after TAC, and that ERKT188-phosphorylation is a central molecular event for nuclear ERK localization and signaling. The gene discussed is MYC; the disease is persistent truncus arteriosus.