Concordant with previous reports in solid tumours [26, 27] and AML [28], guadecitabine upregulated pro-inflammatory signaling, including transcriptional signatures associated with type I and II interferons, TNF-α and the JAK/STAT pathways (Fig. 4E, F and Supplementary Table S6). The gene discussed is SOAT1; the disease is acute myeloid leukemia.