Posttransplantation lymphoproliferative disorder (PTLD) in patients who have undergone solid organ transplantation is thought to be mostly of host (ie, transplant recipient) origin, as opposed to being predominantly of donor origin, which is observed in patients who have undergone bone marrow transplantation. Donor-origin PTLDs reportedly follow a more indolent course than host-origin PTLDs. To determine the origin of PTLD and its clinical implications in patients who have undergone lung transplantation. Patients' medical records were reviewed for clinical data. We performed a molecular study to determine the origin of abnormal lymphoid cells in 4 PTLD cases identified from our autopsy files. Each case underwent restriction fragment length polymorphism analysis using polymerase chain reaction-based genotyping for CYP2D6. Epstein-Barr virus (latent membrane protein 1) immunostaining and polymerase chain reaction analysis were performed on PTLD-involved tissues. Three of 4 PTLD cases were of host origin, and the remaining case was of donor origin. Epstein-Barr virus was detected by immunohistochemical and polymerase chain reaction methods in all PTLD-involved tissues that were examined. There was no apparent difference in clinical manifestations between host-origin and donor-origin PTLD cases in our study. The PTLDs in our patients who had undergone lung transplantation were Epstein-Barr virus-positive and mostly of host origin, without any notable clinical difference from donor-origin PTLD.