The shift from fatty acid oxidation to glycolysis in heart failure is represented by changes in levels of HADH, which regulates fatty acid utilisation (Wang et al., 2022); the downregulation of HADH in iPSC-CMs cultured on plastic compared to 130 kPa PDMS indicates a reduction in the utilisation of fatty acids and breakdown through β-oxidation. The gene discussed is HADH; the disease is heart failure.