As described below in detail, accumulating evidence has revealed multiple cases of hypoxia‐independent activation of HIF1A signaling (Figure 1).8 Indeed, we have recently shown that pseudohypoxia‐mediated HIF1A signaling activation is a central pathobiological mediator of myelodysplastic syndromes (MDS), a group of clonal hematopoietic disorders characterized by ineffective hematopoiesis and multilineage dysplasia.7 This evidence concerns the gene HIF1A and myelodysplastic syndrome.