The verification of the synergy of GC1118 and BEZ-235 in several KRAS-mutant CRC PDX cases less susceptible to GC1118 by high AKT activity is essential to provide clinical reliability and strong support for our hypothesis, highlighting the potential of combined PI3K/mTOR and EGFR inhibition in KRAS-mutant CRC cells with relative high levels of high-affinity EGFR ligands. This evidence concerns the gene KRAS and colorectal carcinoma.