JAK/STAT pathway regulates various cellular functions, including proliferation, apoptosis, differentiation, and aging, thereby contributing to the maintenance of hematologic homeostasis.[53, 54, 55] Although inhibition of the JAK/STAT pathway has been explored as a therapeutic approach for CMML, existing studies mostly focus on the constitutive activation of the pathway due to acquired mutations, such as JAK2V617F. The gene discussed is SOAT1; the disease is chronic myelomonocytic leukemia.