Thus, treating GL15 glioma cells with Lonidamine inactivates the PI3K/AKT pathway, leading to the mitochondrial translocation of p53, the subsequent permeabilization of the mitochondrial membrane, and the release of pro-apoptotic factors like AIF, Bax, Noxa, and Puma, triggering apoptotic cell death [143]. The gene discussed is AKT1; the disease is glioma.