STAT3 activity was restored and stably maintained upon initial ALK-TKIs (alectinib, ceritinib, lorlatinib, and brigatinib) treatment in the absence of ALK signaling (Fig. 1g and Supplementary Fig. 3a), characterizing the treatment-induced adaptive survival of ALK-rearranged lung cancer cells. The gene discussed is STAT3; the disease is lung carcinoma.