Erythrocyte invasion is an essential gateway to malaria disease and a key target for disease intervention. Signaling via the erythrocyte beta 2-adrenergic receptor and heterotrimeric guanine nucleotide-binding protein (Gas) regulates the entry of the human malaria parasite P. falciparum. Disruption of the interaction between the G-alpha-s subunit of the Gs protein and the receptor results in a reduced erythrocyte invasion by the parasite and subsequent low level of parasitemia [28] . Down-regulation in regulator of G-protein signaling in FM patients might be due to some host response to combat this parasitic infection. Conversely, up-regulation of apolipoprotein E was observed in the malaria patients. This apolipoprotein also inhibits Plasmodium invasion, since it shares the cell entry mediators (heparan sulphate proteoglycans and/or low density lipoprotein receptor) with the parasite [29] . The pathway analyses and densely connected networks based on our results provide an insight into the underlying molecular mechanisms of malaria.