Kaposi's sarcoma (KS) is a neoplastic disorder characterized by a highly vascularized lesion with bundles of spindle-shaped cells, pathognomonic of the disease, infiltrated by mononuclear inflammatory and plasma cells. The KS lesion presents as a patch/plaque, which eventually develops into a nodular tumor. Thus far, the mechanisms involved in the etiopathogenesis of KS are not completely understood. Kaposi's Sarcoma-associated Herpesvirus (KSHV) infection is present in all KS cases. However, KSHV is not sufficient for the development of the disease and other factors are certainly involved. Alterations in the expression of cytokines, growth factors and relative receptors have been analyzed over the years.<br/> To evaluate the involvement of FGFR2 in the development and progression of KS, we assayed by immunohistochemistry and quantitative real-time PCR (Q-RT-PCR) the expression of FGFR2-IIIb and FGFR2-IIIc in biopsies of KS lesions compared to normal skin.<br/> Further studies are needed to analyze whether FGFR2-IIIc up-regulation varies in the history of the disease, and whether these variations might correlate with the clinical status of the disorder. In any case, our survey provides new elements to better understand the complex interplay between viral infection and host response in the development of KS.