This observation is consistent with the results of a previous study showing that the accumulation of cardiac amylin is linked to pathological cardiac hypertrophy and diastolic dysfunction where amylin deposit in the nucleus is capable of inducing hypertrophic transcriptional effects, such as activation of Ca2+/calmodulin-dependent protein kinase II (CaMKII)-histone deacetylase (HDAC) and calcineurin-nuclear factor of activated T cells (NFAT) hypertrophic pathways23. Here, HDAC9 is linked to cardiac hypertrophy.