GLUT1 knock-down in the Ccne1+ tumor cells (Fig. 4j, k and Supplementary Fig. 4g, h) did not resolve the exclusion of the CD8+ T cells and did not phenocopy the results obtained with GLUT1 inhibition by BAY-876, suggesting once again that changes in the glycolytic properties of the glyCAF are primarily responsible for the observed increase in T cell tumor infiltration. This evidence concerns the gene SLC2A1 and neoplasm.