On the other hand, conditional deletion of JAK2 in the MPN clone of a mouse model of MPLW515L-driven myelofibrosis-like disease was shown to lead to substantially improved disease modification as compared with JAK inhibitor therapy, providing compelling genetic evidence for continued dependency of key pathological features on constitutive activation of the JAK/STAT pathway in the MPN clone [30]. The gene discussed is SOAT1; the disease is myeloproliferative disorder.