The hypothesis has already been validated in a JAK2-mutated murine model [20], in which the expression of S100A8/A9 heterocomplex provoked inflammation and promoted myelofibrosis, both of which could be reversible upon treatment with a small molecule targeting S100A8/A9 signaling inhibition [20]. Here, IGKV1D-22 is linked to myelofibrosis.