One of the most enthralling aspects of of Plasmodium as a parasite, lies in their ability to invade and remodel the host cell. These processes are mediated in part by the action of the rhoptry proteins, released by specialized secretory organelles viz., the Rhoptries, at the onset of invasion [1]. A major event in remodelling is the establishment of new permeation pathways (NPPs) in the infected red blood cell membrane, so that the parasite can gain access to the nutrients in the serum [1]. The mechanisms by which the parasite is able to establish and regulate these pathways is virtually unknown. Based on the available experimental data we hypothesize that CLAG3 is a constituent of the NPP and that Clag3 interacts with other parasite-encoded proteins as well as host-cell proteins to form the NPP. Since there are multiple CLAG paralogs in P. falciparum and the protein lacks homology to known ion channels in other systems, it is confronting to determine the contribution of CLAG3 in host cell permeability changes [2]. Here, P.falciparum CLAG3 has been functionally analysed using a ribozyme mediated knock down strategy. Attempts have been made to identify the Clag3 interacting partners by mass spectrometry with an aim to understand the molecular makeup of the NPPs and to develop a model for channel activity, which might even have implications in drug resistance. Simultaneously P.berghei CLAGs are also under analysis, which would open up a whole new outlook for nutrient channel structure and function in Plasmodium. Meanwhile the involvement of other important Rhoptry proteins like RhopH2 [3] and RAMA in parasite growth and survival is being investigated, the molecular mechanisms behind the less understood events like remodelling and parasite protein trafficking will hopefully be unravelled in the process.