Depletion of JAK2 in NCI-H1703 cells—which demonstrate the highest levels of STAT3 and pSTAT3Y705 expression—results in a near complete loss of STAT3 phosphorylation comparable to ruxolitinib, supporting the hypothesis that JAK2 is the kinase primarily responsible for STAT3Y705 phosphorylation in NSCLC (Fig. 4C). The gene discussed is JAK2; the disease is non-small cell lung carcinoma.