However, there have been reports of signaling by C5L2 that might not involve G protein activation: in HEK cells, transfected C5L2 can stimulate β-arrestin translocation (Kalant et al., 2005); in mouse neutrophils, C5L2 can modulate the signaling activities of C5aR and the related receptor for C3a, C3aR (Chen et al., 2007) and in a mouse model of sepsis, C5L2 appears to have as important a pro-inflammatory role as C5aR (Rittirsch et al., 2008). This evidence concerns the gene C5AR2 and Sepsis.