Another study showed that the elevation and activation of the Aryl hydrocarbon receptor (AhR) in NSCLC cells could induce JAK2/STAT3 phosphorylation, while the inhibition of JAK2/STAT3 signaling by pharmacologic approaches can attenuate the AhR-mediated stemness effects of NSCLC cells, indicating that the JAK2/STAT3 pathway plays a vital role in AhR-regulated NSCLC stemness [14], and targeting STAT3 has become a promising strategy for lung cancer treatment. Here, JAK2 is linked to lung cancer.