SOAT1 and myelofibrosis: Researchers found that Type I JAKinibs cause cytokine rebounds in cell lines that model myelofibrosis [15,18–20], resulting in pathogenic signaling upon drug withdrawal, particularly in JAK2 V617F myelofibrosis patients [15] who have constitutively active JAK-STAT signaling and resultant increased inflammatory cytokines [21].