Upon hyperactivation of mTORC1 via Tsc2 deletion, increased transendothelial delivery of BODIPY-C16 to tumor cells was observed even in the presence of VEGFR1-Fc, while VEGF-B had no further impact (Supplemental Figure 4F), together indicating that mTORC1 enhances transendothelial LCFA delivery through a VEGF-B–dependent transcytotic mechanism. Here, FLT1 is linked to neoplasm.