FIGURE 1: NIX accelerates cardiomyocyte differentiation. Upregulation of HIF1α activity in response to a variety of stimuli, including hypoxia and developmental signalling, modulates the bioenergetic status of the cell by triggering receptor-mediated mitophagy. These changes allow for the increase in cellular glycolytic capacity necessary to provide energy to drive cardiomyocyte differentiation. Zhao et al. demonstrate that this process is dependent on HIF1α but not on NIX. However, NIX overexpression accelerates the glycolytic shift and leads to early differentiation as evidenced by increased levels of the cardiomyocyte markers MHC and troponin T.