HIF1A and acute myeloid leukemia: Recently, a fully humanized hematopoietic niche system has been exploited to investigate the multidirectional crosstalk among AML, HSCs and the microenvironment and allowed to identify stanniocalcin 1 and its transcriptional regulator HIF-1α as specific mediators whereby AML impairs normal hematopoiesis by remodeling the mesenchymal niche (104).