PPARA, PPARGC1A, and PPARGC1B (Figures 5D–5F), which are involved in the fatty acid oxidation of PLN-KO hiPSC-CMs, began to decline at day 30, while genes involved in glucose utilization, such as GNPNAT1, PGM3, and GFPT1, were upregulated (Figures 5A–5C), indicating that energy metabolism disorders began to occur. The gene discussed is PPARGC1A; the disease is metabolic disease.