Inhibiting EML4-ALK using Alectinib or Lorlatinib resulted in a similar mTOR, p70S6 and ULK1 phosphorylation pattern as seen with Ceritinib treatment (Supplementary Fig. 1C–D).These results suggest that ALK inhibition reduces mTOR activity in H3122 EML4-ALK+ NSCLC cells, and that this leads to activation of ULK1 (via removal of the inhibitory phosphate group at Serine 757), which in turn may lead to initiation of macroautophagy. The gene discussed is EML4; the disease is non-small cell lung carcinoma.