Interestingly, TKI‐treatment did inhibit EGFR tyrosine kinase activity almost completely; however, no inhibitory effect on downstream Akt and ERK pathways was observed in B[α]P‐treated NSCLC cells.93 Cigarette smoke extract and B[α]P both transcriptionally upregulate the activity of the proto‐oncogene c‐MET, also activating its downstream Akt pathway, which could not be targeted by EGFR‐TKIs. Here, AKT1 is linked to non-small cell lung carcinoma.