Interestingly, phosphorylation of the tyrosine-828 residue in the C-terminal cytoplasmic domain of CD133 has been found to mediate direct interactions between CD133 and the phosphoinositide 3-kinase (PI3K) 85 kDa regulatory subunit (p85), resulting in preferential activation of the PI3K/protein kinase B (Akt) pathway in GBM stem cells compared to matched non-stem cells [50]. The gene discussed is PROM1; the disease is glioblastoma.