Fig. 1

JAK2 and CSF3R mutated patients can benefit of ruxolitinb treatment. In basal conditions, JAK2 signaling is initiated by the binding of cytokines to the associated receptors. Once activated, JAK phosphorylates STAT proteins inducing their dimerization and translocation to the nucleus, where they activate or suppress gene transcription. In the presence of JAK2 V617F mutation, the JAK/STAT pathway is constitutively activated. CSF3R is known to signal through the JAK tyrosine kinase pathway. CSF3R membrane proximal mutations, such as T615A, T618I and T640 N, constitutively activate JAK-mediated signaling and are sensitive to its kinase inhibitor ruxolitinib