HIF1A and lymphoid leukemia: Meanwhile, the increase of hypoxia-inducible factor 1α (HIF-1α) in EBV-infected B cells varies across latency programs: LMP1 stimulates the transcriptional activity of HIF-1α through the p42/44 MAPK pathway and contributed to its stabilization [33, 34]; both LMP1 and EBNA1 upregulated HIF-1α and its downstream targets IL-8 and VEGF [35]; EBNA3s expressed in lymphoid chronic leukemia bind prolyl hydroxylases (PHD1 and PHD2) and block their phosphorylation activity, thereby stabilizing HIF-1α [36].