This novel function for Mcl-1, distinct from its anti-apoptotic function may explain the observed heart failure in Mcl-1 null mice, in which cardiomyocytes exhibited aberrant mitochondrial structure and defects in respiration that were not rescued by Bax/Bak deletion (100), although the defects were partially rescued by deletion of cyclophilin D, a key regulator of the mitochondrial permeability transition pore (101). This evidence concerns the gene MCL1 and heart failure.