The data with cardiomyocyte-specific BRAFV600E knock-in are consistent with compensated, concentric hypertrophy in mice with cardiomyocyte-specific expression of constitutively-active MKK1 [46], and in accord with studies of mice with deletion of ERK1 and/or ERK2 in heart failure models showing that ERK1/2 signalling is cardioprotective and required for concentric hypertrophy [47]. This evidence concerns the gene MAPK1 and heart failure.