The involvement of PI3K/AKT signalling in glioma is known in terms of regulating the ability of cells to divide, migrate, invade and undergo angiogenesis.41, 42 Oncogenesis caused by FGFR1 was earlier shown to be associated with PI3K/AKT signalling pathway.43 Our findings showed inhibition of PI3K/AKT pathway by overexpressed miR‐3116, while overexpressed FGFR1 showed opposite results in addition to reversing the suppression of PI3K/AKT signalling caused by miR‐3116. The gene discussed is AKT1; the disease is central nervous system cancer.