Taken together, this suggests that, in addition to their increased presence in AOM/DSS tumors, Phd2-deficient macrophages display protumorigenic features and increased Ereg expression in vitro, which implies a mechanistic link to the observed increase in oncogenic STAT3 and ERK1/2 signaling in Phd2+/– tumors in vivo. The gene discussed is EREG; the disease is infectious otitis media.