PTEN is a tumor suppressor that negatively regulates the PI3K/AKT signaling pathway, and PTEN can regulate cardiac hypertrophy and survival.[10] To explore the function of Pten in cardiomyocyte differentiation, we generated Pten‐deficient mouse ESCs using the CRISPR‐Cas9 system as described previously.[29] Cardiomyocytes were generated from wild‐type (WT) and Pten−/− ESCs using the differentiation protocol described above. The gene discussed is AKT1; the disease is neoplasm.