Phosphorylated-CaMKII increased the output of HDAC4, HDAC5, and HDAC7 from the nucleus, decreasing their inhibitory effect on the activity of MEF2 transcription factors, and promoting pathological left ventricular hypertrophy markers Brain Natriuretic Peptide and α-SK gene transcription, leading to cardiovascular dysfunction.78 Further work is needed to identify sex differences in CaMKP expression and related signaling processes in cardiomyocytes and the molecular mechanisms upstream of this sex-specific CaMKP compartmentalization after TAC. The gene discussed is PPM1F; the disease is persistent truncus arteriosus.