In support of this, the homozygous deletion of Drp1 in mice is responsible for embryonic lethality, which is due to elongated mitochondria, altered apoptosis and reduced cell proliferation, while postnatal cardiac specific knock out of Drp1 leads to dilated cardiomyopathy and rapid lethality in mice [117, 118]. The gene discussed is DNM1L; the disease is dilated cardiomyopathy.