The observation of thrombocytosis is consistent with the role of SH2B3 as a negative regulator of JAK/STAT signaling as previously demonstrated [4, 10, 12], also demonstrated by the increase in megakaryocytic progenitors, megakaryocytes, and platelets in hematopoietic tissue, along with an increase in erythroid progenitors, reported in Sh2b3-deficient mice [27]. Here, SH2B3 is linked to thrombocytosis disease.