In the future, it will be important to evaluate PI3K p110α inhibition in CRC cells with alternative mutational patterns including: distinct hotspot mutations in KRAS and PIK3CA, NRAS mutations, BRAF mutations as well as wild type KRAS. In addition, combination of PI3K p110α inhibition with other targeted therapies, namely anti-EGFR antibodies, could provide alternative and improved therapeutic strategies that would be particularly interesting in the context of drug resistance. This evidence concerns the gene BRAF and colorectal carcinoma.