Moreover, genes that were higher in C/ebp-targeted tumors were enriched among the genes that were higher within the indeterminate population, thus reinforcing the notion that the indeterminate state corresponds to progenitor-like cells exhibiting low C/EBP activity (Fig. 6b). These analyses uncovered shared transcriptional changes upon inactivation of either C/ebp factors or Lkb1, suggesting that C/EBPs may operate downstream of LKB1 to suppress tumor growth and maintain ATII identity. The gene discussed is STK11; the disease is neoplasm.