Additionally, the use of G-CSF after allogeneic HCT is not well established, with heightened risk of graft-versus-host disease.1–3 G-CSF is a growth factor that can stimulate the expression of interleukin-1 (IL-1), interleukin-6 (IL-6), tumour necrosis factor (TNF)-α mediators and myeloid cell recovery, leading to a potential exuberant inflammatory response during the immune reconstitution and engraftment after transplantation. Here, CSF3 is linked to graft versus host disease.