The solid tumor microenvironment (TME) impairs the metabolic function of tumor-infiltrating CD8+ T cells, limiting their ability to maintain energy for antitumor activity. CD8+ T cells in the TME rely on mitochondrial fatty acid oxidation (FAO) for energy, but endogenous T cells and unmodified cellular therapies fail to sustain bioenergetics. The study reveals that the TME maintains perpetual acetyl-CoA carboxylase (ACC) activity, promoting lipid biosynthesis and storage in T cells, which opposes FAO. Restricting ACC rewires T cell metabolism, enabling energy maintenance in the TME. Limiting ACC activity enhances T cell longevity and polyfunctionality, improving cancer control. ACC1 is induced in CD8+ TILs, promoting lipid storage and restricting FAO. ACC inhibition reduces lipid accumulation, increases FAO, and enhances T cell function. ACC1 deletion or inhibition in T cells leads to reduced lipid storage, increased FAO, and improved T cell survival. ACC inhibition promotes T cell memory traits and enhances antitumor immunity. ACC activity in T cells is linked to lipid metabolism and bioenergetics, with ACC1 playing a key role in regulating T cell metabolism. ACC inhibition improves T cell function in the TME, suggesting that targeting ACC could enhance T cell-based immunotherapies. The study highlights the importance of ACC in regulating T cell metabolism and lipid utilization in the TME, offering a potential strategy to improve cancer immunotherapy.The solid tumor microenvironment (TME) impairs the metabolic function of tumor-infiltrating CD8+ T cells, limiting their ability to maintain energy for antitumor activity. CD8+ T cells in the TME rely on mitochondrial fatty acid oxidation (FAO) for energy, but endogenous T cells and unmodified cellular therapies fail to sustain bioenergetics. The study reveals that the TME maintains perpetual acetyl-CoA carboxylase (ACC) activity, promoting lipid biosynthesis and storage in T cells, which opposes FAO. Restricting ACC rewires T cell metabolism, enabling energy maintenance in the TME. Limiting ACC activity enhances T cell longevity and polyfunctionality, improving cancer control. ACC1 is induced in CD8+ TILs, promoting lipid storage and restricting FAO. ACC inhibition reduces lipid accumulation, increases FAO, and enhances T cell function. ACC1 deletion or inhibition in T cells leads to reduced lipid storage, increased FAO, and improved T cell survival. ACC inhibition promotes T cell memory traits and enhances antitumor immunity. ACC activity in T cells is linked to lipid metabolism and bioenergetics, with ACC1 playing a key role in regulating T cell metabolism. ACC inhibition improves T cell function in the TME, suggesting that targeting ACC could enhance T cell-based immunotherapies. The study highlights the importance of ACC in regulating T cell metabolism and lipid utilization in the TME, offering a potential strategy to improve cancer immunotherapy.