NFATC4 and cardiac hypertrophy: This activation of p38 affects de-phosphorylated NFATc4 by re-phosphorylation that antagonizes the Ca2+-mediated de-phosphorylation and nuclear translocation of NFATc4, which results in NFATc4 being exported out of the nucleus and termination of NFATc4-mediated transcription [23], [32], [34], hence cardiac hypertrophy signaling.