Studies by the Miggliacio group supported this concept by demonstrating that impaired Mk maturation in the GATA1low animal model of myelofibrosis leads to abnormal P-Selectin distribution and emperipolesis (91), raising the possibility that neutrophil proteases might facilitate the pathological release/activation of Mk α-granule proteins and growth factors, such as TGF-β, which are critical in the pathogenesis of myelofibrosis (92). This evidence concerns the gene SELP and myelofibrosis.