We corroborated these findings in GBM by demonstrating that CD97+ single-cell clusters had increased transcription of genes involved in the ERK/MAPK and PI3K/AKT pathways than CD97- clusters, patient GBMs with overall highest levels of CD97 expression had activation of similar pathways, and CD97 knockout in a GBM cell line decreased PI3K/AKT activation. The gene discussed is AKT1; the disease is glioblastoma.