Our studies extend the phenotypic spectrum of disordersresulting from mutations of Rho GTPases and specifically implicate the CDC42 R186Cmutation in altering interactions of hematopoietic cells with the microenvironment.Moreover, studies of acquired primary myelofibrosis suggest that disruption of CDC42may occur in hematopoietic progenitor cells in this disease, connecting theobservations made in these rare cases to the pathogenesis of other, more common,acquired malignant hematopoietic disorders. This evidence concerns the gene CDC42 and myelofibrosis.