The solid tumor microenvironment (TME) impairs the metabolic state of tumor-infiltrating T cells (TILs), leading to reduced energy synthesis and survival. T cells in the TME must rely on mitochondrial fatty acid oxidation (FAO) to generate energy under nutrient stress, but endogenous TILs and unmodified cellular therapy products often fail to maintain bioenergetics in tumors. This study reveals that the TME induces persistent acetyl-CoA carboxylase (ACC) activity, promoting lipid biogenesis and storage in TILs, which opposes FAO. Using metabolic, lipidomic, and confocal imaging strategies, the authors found that restricting ACC rewires T cell metabolism, enabling energy maintenance in the TME. Inhibition of ACC activity enhances a gene and phenotypic program indicative of T cell longevity, increasing survival and polyfunctionality, which supports cancer control. The findings suggest that targeting ACC could be a potential strategy to enhance the efficacy of T cell-based immunotherapies in solid cancers.The solid tumor microenvironment (TME) impairs the metabolic state of tumor-infiltrating T cells (TILs), leading to reduced energy synthesis and survival. T cells in the TME must rely on mitochondrial fatty acid oxidation (FAO) to generate energy under nutrient stress, but endogenous TILs and unmodified cellular therapy products often fail to maintain bioenergetics in tumors. This study reveals that the TME induces persistent acetyl-CoA carboxylase (ACC) activity, promoting lipid biogenesis and storage in TILs, which opposes FAO. Using metabolic, lipidomic, and confocal imaging strategies, the authors found that restricting ACC rewires T cell metabolism, enabling energy maintenance in the TME. Inhibition of ACC activity enhances a gene and phenotypic program indicative of T cell longevity, increasing survival and polyfunctionality, which supports cancer control. The findings suggest that targeting ACC could be a potential strategy to enhance the efficacy of T cell-based immunotherapies in solid cancers.