Tvorogov et al. (2018) suggested that ruxolitinib binding promotes pJAK2 accumulation by preventing JAK2 dephosphorylation and degradation (Tvorogov et al., 2018; Ross et al., 2021). Despite the dose-dependent toxicity, low efficacy and the withdrawal syndrome associated with ruxolitinib therapy in MPNs, ruxolitinib remains the best available therapy (BAT) for MF and therefore, may be beneficial for ALL patients harboring JAK2 alterations. The gene discussed is JAK2; the disease is acute lymphoblastic leukemia.