The functional consequences of the reciprocal regulation of α-MHC and β-MHC during cardiac remodeling, not obligatory coupled at the level of individual cardiomyocytes [30], is subjected of debate between those considering that this qualitative change actively contributes to heart failure and those suggesting that it represents a compensatory mechanism allowing the cardiomyocyte to be more energy-efficient [31]. The gene discussed is HLA-C; the disease is heart failure.