In a mouse model of JAK2 and IDH2 co-mutated MPN, combined inhibition of JAK2 and IDH2 (with ruxolitinib and enasidenib, respectively) normalized reduced disease burden to a greater extent than JAK inhibition alone by reversing aberrant gene expression and metabolite perturbation in the hematopoietic stem cell compartment [143]. This evidence concerns the gene JAK2 and myeloproliferative disorder.