This was revealed by the considerable decrease in EGFR, PI3K, and AKT activities and the epithelial intercellular transition via the suppression of fibronectin and vimentin downstream of the EGFR/PI3K/AKT signaling pathway to inhibit cell invasion and migration, in addition to an increase in P21 production to promote apoptosis.41, 42 This not only clarified the linc00152 mechanism related to the progression of NSCLC but also suggests that linc00152 is a potential therapeutic target. The gene discussed is EGFR; the disease is non-small cell lung carcinoma.