However, it is contested if elevated cardiac Ankrd1 levels alone promote the development of cardiomyopathy, as two independent studies using transgenic Ankrd1 mice gave opposing results: one finding no overt physiological abnormality of transgenic mice, while the other showed diastolic dysfunction (by shifting the titin isoforms ratio towards the stiffer N2B version) and progressive heart failure (Piroddi et al. 2020; Song et al. 2012). The gene discussed is ANKRD1; the disease is cardiomyopathy.