Although only one case was tested in the present study, our data highlight the potential of combined PI3K/mTOR and EGFR inhibition for KRAS-mutant CRC cells with relatively high levels of high-affinity EGFR ligands, although further investigation on the therapeutic efficacy, mode of action, and tolerability of this combination based on additional KRAS-mutant PDX models concurrently harboring other genetic alterations (with different genetic backgrounds) is required. This evidence concerns the gene EGFR and colorectal carcinoma.