The study of mice mDia1 heterozygous or homozygous showed that mDia1 deficiency led to a cell-autonomous overexpression of the membrane antigen CD14 and a hypersensitive innate immune response mediated by CD14/TLR4-like signaling; these mice develop age-dependent MDS that is accelerated by chronic stimulation of innate immunity [67]. Here, CD14 is linked to myelodysplastic syndrome.