4I-K). Analysis of these samples using ATAC-seq revealed reduced chromatin accessibility in the TAP2 gene promoter region spanning ± 3 kb around the transcription starting site in NSCLC as compared to non-tumor lung tissue, supporting epigenetic silencing of TAP2 (Fig. 4L). The sequence analysis of the promoter sites with differential accessibility in malignant vs nonmalignant samples identified numerous consensus motifs for binding of transcription factors involved in proinflammatory responses including HDAC2, IRF1, EGR1, STAT1, MYC, GTF3C2, HIF1A and STAT2 (Fig. 4M). The gene discussed is TAP2; the disease is neoplasm.