Although we focused on CRC PDX cases harboring only KRAS mutations to validate the potential of combined PI3K/mTOR/AKT and EGFR inhibition in KRAS-mutant CRC cells with high AKT activity due to several mechanisms such as the ratio of high- to low-affinity EGFR ligands, further investigations on CRC PDXs harboring concurrent mutations in both KRAS and the genes activating PI3K/mTOR/AKT pathway (e.g., PIK3CA) are required to strengthen the importance of PI3K/mTOR/AKT pathway in the resistance to GC-1118. This evidence concerns the gene EGFR and colorectal carcinoma.