AKT1 and glioblastoma: The results (Figure 1C and 1D) showed that CH12 attenuated the phosphorylation of EGFR, AKT and ERK, and that it also inhibited the phosphorylation of STAT5, a transcription factor, regulating gene expression when stimulated by a wide variety of growth factors, hormones, and cytokines and contributing to proliferation in human GBM tumors [31–32].