The findings thus demonstrated that the compound luteolin in A549 lung adenocarcinoma cells exerted and proliferation protective effect in a dose as well as time‐related manner caused occurrence of apoptosis with a related increase in the activation of caspases (9 and 3), Bcl‐2 dimunition, Bax expression elevation, MEK phosphorylation along with its downstream kinase namely ERK and the activation of Akt. Luteolin also substantially repressed the migration and motility in A549 cell (Meng, González‐Abuín, Pinent, Ardévol, & Blay, 2016). The gene discussed is BCL2; the disease is lung adenocarcinoma.