In contrast, mice with deletion of HIF1A in vascular endothelia (Hif1af/f CadherinCre+; Figure 7B, Figure S5A), myeloid cells (Hif1af/f LysozymCre+; Figure 7C) [70], or the conducting airways (Hif1af/f ClaraCellCre+; Figure 7D, Figure S5B) [71] showed no difference in survival time, pulmonary edema, or gas-exchange during ALI as compared to corresponding controls. This evidence concerns the gene HIF1A and acute respiratory distress syndrome.