EGR1 and cardiac hypertrophy: Although its expression level is low in quiescent states, ATF3 expression is induced in response to stress conditions such as DNA damage, stimulation with cytokines or chemokines, or exposure to toxins, hypoxia, or ischemia/reperfusion injury.50, 51, 52 The roles of ATF3 in the cardiovascular system, however, are somewhat controversial; for example, ablation of ATF3 has been shown to exaggerate cardiac hypertrophy via ERK/c-Jun N-terminal kinase (JNK)53 or Egr1,54 whereas its overexpression also induces cardiac hypertrophy and arrhythmia.55