However, the idea that ACKR3 is merely a scavenger receptor modulating CXCR4 function and an ACKR not coupled to classical G protein signaling was in turn challenged by Ödemis et al., who showed that ACKR3-mediated effects on ERK and AKT activation in rodent astrocytes and human glioma cells were pertussis toxin-sensitive, and hence mediated by G protein activation (217). This evidence concerns the gene CXCR4 and glioma.