In addition, the published studies reveal that the deficiency in Lnk has shown advanced JAK/STAT signaling in a cytokine-independent manner and the increased ability of oncogenic JAK2 to promote the expansion of myeloid progenitors both in vitro and in vivo.252 Moreover, JAK inhibitors inhibit Lnk-deficient cell lines, suggesting that the treatment of JAK2 inhibitors may be a novel choice for MPN patients with Lnk deficiency. The gene discussed is SOAT1; the disease is myeloproliferative disorder.