Because IP3-sensitive release of Ca2+ from perinuclear Ca2+ stores is reported to activate two Ca2+-dependent hypertrophic pathways (calcineurin/nuclear factor of activated T-cells (NFAT) [8] and the Ca2+/calmodulin-dependent protein kinase II (CaMKII)/histone deacetylase (HDAC) pathways [3]), receptor stimulation-elicited [Ca2+] elevation in the nucleus observed in this study would contribute to the gene transcription program that precedes cardiac hypertrophy (Fig 7). This evidence concerns the gene HDAC9 and cardiac hypertrophy.