The fact that LRIM1 has been linked to the TEP1/APL1 anti-Plasmodium mechanism [33], [34] suggests that it is very likely to play a role in anti-Plasmodium activity, but it is possible that it may not be required (or is redundant) at very low infection intensities, or that RNAi-mediated depletion is not be sufficient to reduce it to a level that would have any impact on a low-intensity infection. This evidence concerns the gene TEP1 and infection.