The upregulation of ALKBH5 transcription by the adeno-associated virus type 9 (AAV9) enhanced the percentage of replicating cardiac cells, decreased scar diameters, and normalized cardiac function following infarction damage, whereas ALKBH5 knockout in mice significantly restricted the rate of cardiomyocyte propagation and healing [179]. The gene discussed is ALKBH5; the disease is infarction.