At the level of the cardiac sarcomere, as cTnI (TNNI3 gene product) progressively replaces ssTnI (TNNI1) during maturation, there is no reactivation of the fetal TNNI1 gene program, even in disease states including stress, hypertrophy (physiological or maladaptive), ischemia, or in heart failure (Bhavsar et al., 1991; Solaro, 1999). Here, TNNI3 is linked to heart failure.