Notably, alterations of the RTK/RAS/PI3K pathway, found in 90% of GBM, are also driven by mutations in the PI3K catalytic subunit PIK3CA [60], as described in patient-derived xenograft mice models harboring mutant PIK3CA, in which gliomagenesis and neuronal hyperactivity showed a reciprocal influence, likely through a secreted factor (e.g., glypican 3, GPC3), selectively expressed in these tumors [71]. This evidence concerns the gene GPC3 and glioblastoma.