Abstract Kaposi sarcoma (KS) is a multicentric neoplasm of lymphatic endothelium derived cells infected with Kaposi's human herpesvirus 8 (HHV8). Post-transplant KS can lead to multifocal, progressive (florid) lesions with frequent primary involvement of the oral mucosa and dissemination to the viscera. KS prevalence after organ transplantation varies greatly depending on the prevalence of HHV8 infection in the general population. Most cases of post-transplant KS develop as a result of viral reactivation. Immunohistochemistry using a monoclonal antibody against HHV8 latent nuclear antigen on paraffin embedded sections, although less sensitive than polymerase chain reaction, is useful for pathological diagnosis of difficult angiogenic proliferations. Although HHV8 viral load in peripheral blood mononuclear cells of KS individuals correlates with tumor burden, due to low interval variations this test cannot be used in clinical practice to monitor KS patients nor to predict the occurrence of KS in transplant recipients. The main objectives of KS treatment is to control disease progression and relieve symptoms, as opposed to achieving complete tumor remission. The cornerstone in treatment of post-transplant KS is to taper down immunosuppressive regimens to the lowest possible level, while attempting to keep the allograft functional. Specific local or, less frequently, systemic treatment modalities can be used such as chemotheraphy. Other therapeutic strategies could rely in targeting signaling pathways important for HHV8 de novo infection, reaction, cell persistence or cellular pathways activated by viral pirated genes such as the mitogen-activated protein kinase or the PI3 kinase pathway. Rapamycin, a mammalian target of rapamycin inhibitor located downstream the PI3 kinase, has already proven of benefit and should be discussed in all post-transplant KS.