Albini et al (1999) made the observation that the in vivo administration of somatostatin decreases the development of KS-like lesions in mice inoculated with KSIMM cells, despite an absence of somatostatin receptors on the tumoral cell surface. In the light of our data on the effect of IGF-I in these cells, we speculate that somatostatin, by inhibiting pituitary GH release, may also have had an antitumoral effect via a decrease in endocrine IGF-I, as it was demonstrated for other tumors (Wu et al, 2003). This evidence concerns the gene GH1 and Kaposi's sarcoma.