Therefore, we here aimed to study the role of myeloid cell HIF1α in the host defense during pneumonia-derived sepsis using a well-established model via low-dose infection with K. pneumoniae via the airways [17–19], resulting in a gradually growing bacterial load in the lungs with subsequent dissemination and sepsis, allowing analyses of both early protective and late injurious responses associated with innate immune activation. The gene discussed is HIF1A; the disease is infection.