Accumulation of long-chain fatty acids in TME can inhibit the mitochondrial function of CD8+TILs in pancreatic ductal adenocarcinoma and trigger the major transcriptional reprogramming of the lipid metabolism pathway, thereby leading to the reduction in fatty acid catabolic metabolism and inducing CD8+TIL depletion, thus inhibiting T cell activity [68]. This evidence concerns the gene CD8A and pancreatic ductal adenocarcinoma.