Specifically, progenitor-like cells significantly upregulated Cdkn2a relative to other premalignant cells (Fig. S3c,d), and inspection of splice junctions in sequencing reads indicated that transcripts encoding both p19ARF and p16INK4A were induced (Fig. S3e), indicating that both tumor suppressive programs encoded by the Cdkn2a locus were engaged19,41. The gene discussed is CDKN2A; the disease is neoplasm.