There is a growing body of evidence that platelets (PL) are involved in CM pathogenesis: (i) thrombocytopenia is marked during P. falciparum and experimental CM; (ii) PL adhesion to the microvessels has been associated with CM in humans [4], and has been shown to be involved in mouse CM pathogenesis [4], [5]; (iii) in vitro co-cultures showed that PL act as a bridge between pRBC and TNF-stimulated endothelium, and contribute to brain endothelial alterations [6], [7]. The gene discussed is TNF; the disease is cutaneous mastocytosis.