For instance, during pancreatitis, well-differentiated acinar cells generate a metaplastic population with transcriptional features that are intermediate for acinar (Zg16, Cpa1) and tumorigenesis-associated (S100a6) programs within 24 hpi (ADM-PDAC “Bridge”) (Fig. S3F), and Nes+ progenitor-like cells shift into a state showing reduced activation of tumor suppressive programs (Cdkn2a). This evidence concerns the gene CDKN2A and pancreatitis.