Currently, new advances have been made in the field of Tim-3-mediated regulation of immune inflammation in heart failure; Yu et al. (17) discovered that the proportion of Tim-3 on CD4+ and CD8+ T cells was significantly increased in patients with chronic heart failure, suggesting that Tim-3 may induce T cell dysfunction in patients with chronic heart failure, participate in the process of myocardial remodeling, and accelerate heart failure progression. Here, HAVCR2 is linked to heart failure.