To test the hypothesis that TAMs are crucial for promoting Phd2-deficient tumor growth in CAC, we used transgenic Vav:Cre-Phd2fl/fl mice that harbor a homozygous deletion of Phd2 in all hematopoietic lineages (including macrophages) and subjected them to AOM/DSS treatment. This evidence concerns the gene EGLN1 and infectious otitis media.