Finally, we observed significant enrichment of the autophagy/lysosomal transcriptional program upon FGFR inhibition (or dual FGFR/EGFR inhibition) (Fig. 4m and Supplementary Fig. 7j, k), reminiscent of the adaptive upregulation of autophagy/lysosomal activity observed as a protective response to KRAS-MEK inhibition in pancreatic cancer cells38–40. The gene discussed is EGFR; the disease is pancreatic neoplasm.