According to the data available, one of the consequences that resulted in permanent silibinin-induced inactivation of typically proliferative signaling in cervical cancer cells requires the inhibition of mTOR pathways [25], directed at the mTOR pathways and adjusting the activity of Akt, silibinin proves to be a promising drug in the direction of suppressing the tumor and increasing the number of cell deaths. The gene discussed is AKT1; the disease is neoplasm.