Emerging evidence has demonstrated that metabolic crosstalk initiated by tumor cells has crucial effects on the functional dynamics of CD8+ T-cell-mediated antitumor ability.24 Recent studies have elucidated connections between T-cell dysfunction and tumor cells through discrete facets, such as amino acid communication and glucose metabolic reprogramming.25,26 However, the influence of intratumor regulatory element-mediated lipid metabolic plasticity, particularly PUFA homeostasis, on CD8+ T-cell effector functions requires comprehensive elucidation. This evidence concerns the gene CD8A and neoplasm.