While BODIPY-C16 transport was significantly reduced in Rptor-KO endothelial cells, Clstn1 knockdown did not further alter BODIPY-C16 intensity in tumor cells (Figure 4E and Supplemental Figure 5G), suggesting that CLSTN1 functions downstream of mTORC1 to support transendothelial LCFA transport. This evidence concerns the gene RPTOR and neoplasm.