For example, in colorectal cancer, coexistant K-Ras and PI3K mutations decrease sensitivity to PI3K and mTOR inhibition [158], and in lung cancer, the addition of a constitutively active PI3K mutant to epidermal growth factor receptor (EGFR) mutant tumors confers gefitinib resistance in vitro [160]. Here, KRAS is linked to lung carcinoma.