In keeping with this, our interrogation of ICGC and TCGA databases revealed that a hypoxia transcriptional signature is upregulated in PDAC tumours with inactivation of KDM6A. We explored this signature and identified GLUT1 as a biomarker that links hypoxia to KDM6A status in PDAC, and leveraged this information to verify if similar mechanisms were operating in SPNs. The gene discussed is KDM6A; the disease is neoplasm.