Similarly, Myc—basal expression of which is required for Kras-driven lung tumor initiation53 and overexpression of which is sufficient to induce lung tumorigenesis54—showed increased looping between its promoter and two putative downstream enhancers (Extended Data Fig. 8e,f) and increased scA/B scores (Extended Data Fig. 8g) in the AT2-to-adenoma transition, concordant with increased expression. The gene discussed is MYC; the disease is adenoma.