Overall, contrasting MNP- and T-cell phenotypes in acute and chronic GvHD potentially reflects differences in disease pathogenesis and pathophysiology: aGvHD develops upon barrier dysfunction and dysbiosis after conditioning therapy,56 and the subsequent IL-4-containing cytokine milieu57 may induce skin homing of donor monocyte-derived MΦs with tissue-remodelling properties. The gene discussed is IL4; the disease is graft versus host disease.