To assess the putative functions of PHD1–3 in CAC, we employed the AOM/DSS model (26) in Phd1-, Phd2-, or Phd3-deficient (Phd1–/–, Phd2+/–, and Phd3–/–) mice and WT controls; after AOM-induced epithelial mutagenesis, mice underwent repeated cycles of DSS exposure followed by a recovery period (Figure 1A). This evidence concerns the gene EGLN3 and infectious otitis media.