Last, we excluded that the increased infiltration of Rapa-CD8CAR cells into our tumor models was due to altered expression of cell adhesion molecules (CD62L, CD49d, CD2, CD44, CD103, CD11a, LPAM-1) and chemokine receptors (CCR5, CXCR3, CXCR4, CCR7, CCR3), whose levels were not altered compared to ctrl-CD8CAR cells (Supplementary Fig. 10G), reinforcing the importance of the metabolic reprogramming induced by rapamycin to promote CAR T cell infiltration. This evidence concerns the gene TRERF1 and neoplasm.