Preclinical experiments have suggested that PI3K pathway alterations may predict a differential response to PI3K inhibitors in models of nonsmall cell lung cancer (NSCLC),7 and PI3K pathway activation has been identified as one of the factors driving resistance to EGFR TKIs in preclinical models.8 An ongoing phase II study (NCT01297491) is therefore evaluating single-agent buparlisib versus docetaxel or pemetrexed in patients with squamous or nonsquamous metastatic NSCLC with PI3K pathway alterations (PIK3CA mutation and/or PTEN alteration). The gene discussed is EGFR; the disease is lung cancer.