Consistently, in hepatocellular carcinoma (HCC) models, modulation of CD155 had no effect on ERK activation but led to changes in p38 MAPK signaling.45 In contrast, in glioma cells, siRNA-mediated knockdown of CD155 did not affect ERK or AKT phosphorylation but specifically disrupted Src/PXN signaling.17 These findings indicate that CD155-driven signaling may vary across tumor types and involve alternative regulatory networks beyond the canonical AKT/ERK signaling. This evidence concerns the gene SRC and glioma.