In MPN preclinical models, the JAK2-dependent cells survive despite chronic JAK2 inhibition through “JAKi persistence”, which involves the reactivation of JAK/STAT signaling through heterodimerization between JAK2 and JAK1 or TYK2, followed by trans-phosphorylation of JAK2. This evidence concerns the gene JAK1 and myeloproliferative neoplasm.