In NSCLC, the early-phase clinical trials of PI3K inhibitors and dual PI3K/mTOR inhibitors have yielded negative results.16–18 The modest therapeutic efficacy of PI3K inhibitors may be attributed to various reasons, including insufficient target inhibition, intrinsic and acquired drug resistance, and tolerability.106 Unlike other oncogenes, such as EGFR in LUAD, the correlation between specific PI3K pathway mutations and drug sensitivity is not absolute.107 This makes patient selection more complicated based on PI3K pathway mutation status. This evidence concerns the gene EGFR and non-small cell lung carcinoma.