Furthermore, by longitudinally analyzing the CD45.2+ ACC1-knockout CD8+ cytotoxic T lymphocytes (CTLs) transferred to CD45.1+ recipient mice, ACC1 deficiency is proved to hamper CTLs proliferation and activation, and upon Listeria monocytogenes OVA (LmOVA) infection, the survival and accumulation of antigen-specific CTLs, whereas in vitro supplementation of FAs can restore CTL stable survival and the potential of blastogenesis, suggesting a crucial role of de novo FAS for CTL as well [95]. The gene discussed is ACACA; the disease is infection.