Premature T-cell failure may accelerate aging in multiple organs and systems, with thymic degeneration, mitochondrial dysfunction, genetic and epigenetic alterations, and imbalance in protein homeostasis being the four main hallmarks of T-cell senescence.161 Desdín-Micó G et al. reported that in mice with mitochondrial transcription factor A (TFAM) deletion, T cells with mitochondrial dysfunction induce a variety of aging-related phenotypes, such as metabolic disorders, cognitive impairment, and cardiovascular diseases, which ultimately lead to the premature death of mice.162. The gene discussed is TFAM; the disease is cardiovascular disorder.