Human cardiac troponin I (TNNI3) is known to be phosphorylated at multiple amino acid residue sites by several kinases. Protein kinase A (PRKACA) can phosphorylate serine 23 and 24 sites on TNNI3. Phosphorylation of TNNI3 reduces myofilament calcium sensitivity (Mittmann et al. 1990, Keane et al. 1997, Zhang et al. 2012). Defects in TNNI3 can cause a range of cardiomyopathies (Lu et al. 2013). The ATP2B4:NOS1 complex, via cAMP, increases PRKACA activity, thereby regulating the response of the heart to beta-adrenergic agonists.