The engagement of specific immune checkpoints or adhesion molecules could trigger signaling pathways within cancer cells that lead to increased expression of MLXIPL. (3) The infiltration of CD8+ T cells and their interaction with other components of the TME, such as fibroblasts, endothelial cells, and other immune cells, could lead to changes in the TME that indirectly promote MLXIPL expression in cancer cells. The gene discussed is CD8A; the disease is cancer.