The convergence of JAK2 and compensatory RAS signaling during JAK2 inhibitor resistance on the inactivation of BAD function, which would leave the anti-apoptotic activity of BCL-2 proteins intact, nicely complements the promising early results of ongoing clinical studies assessing BCL-2 family inhibition with navitoclax in combination with ruxolitinib in myelofibrosis [54]. The gene discussed is BAD; the disease is myelofibrosis.