As no significant differences were detected in the cell-cycle rates of miR-222-overexpressing cells treated or not with the AKT inhibitor BKM120 (Fig. 7a), we considered the capability of miR-222 to overcome the inhibition of the PI3K/AKT pathway, on one side considering the frequent constitutive activation of the MAPK axis, on the other the number of genes inhibiting proliferation, inducing apoptosis or generally playing tumor suppressor functions, known to be directly targeted by miR-222 [14]. Here, AKT1 is linked to neoplasm.