By globally regulating lysosomal genesis and the ALP, TFEB is pivotal for the cell to manage IPTS (Wang and Cui, 2017); hence, a better understanding of the full time course of myocardial TFEB expression and activity changes in a bona fide animal model of cardiac IPTS should guide the effort for the development of more precise therapeutic strategies for heart disease with IPTS, to which a large subset of heart failure belongs (Sandri and Robbins, 2014; Zech et al., 2019). The gene discussed is TFEB; the disease is heart disorder.