It seems that these effects may be enhanced in EGFR-driven adenocarcinoma, especially by the L858R mutation in exon 21, and that the involvement of AhR is restricted to PAH-mediated activation, since dioxins may not activate EGFR to a similar extent and unliganded constitutive AhR appears to suppress lung tumor progression independent of the driver mutation. The gene discussed is EGFR; the disease is pulmonary arterial hypertension.