For example, the presence of a KRAS mutation and the mutant p110 subunit of PI3K in the patients with advanced CRC results in a clinical resistance to anti-EGFR therapy such as monoclonal antibodies cetuximab and panitumumab [70,71] because both KRAS and PI3K are downstream targets of the EGFR pathway (Figure 1). The gene discussed is EGFR; the disease is colorectal carcinoma.