Passaro et al. (2017) showed this remodeling to differentially involve an increase in arteriolar (CD31+Sca1high) ECs, but loss of those corresponding to sinusoids (CD31+Sca1low). Remodeling was associated with disrupted sinusoidal structure, reduced overall vessel diameter, increased vascular permeability, and induction of poorly perfused, hypoxic regions; initially co-localizing with AML cells but becoming more pervasive throughout marrow with higher levels of leukemic marrow infiltration (Passaro et al., 2017). This evidence concerns the gene PECAM1 and acute myeloid leukemia.