AKT1 and glioblastoma: Here we provide evidence that one of such mechanisms can be miRNA‐483‐3p overexpression, which mainly results in upregulated expression and signaling activity of ERBB3, a prominent regulator of stem‐like cells in CRC [7] and in glioblastoma, where ERBB3 specifically sustains the PI3K/AKT axis [46].