As phosphorylated BAD prevents it from negating the anti-apoptotic activity of BCL-2 family proteins [101, 102], the assessment of the BCL-2 protein inhibitor navitoclax in ongoing clinical studies [54] with ruxolitinib in myelofibrosis patients is relevant to the finding that BAD phosphorylation/inactivation plays a role in JAK2 inhibitor persistence [66, 83]. This evidence concerns the gene JAK2 and myelofibrosis.