To understand the signaling interplay and the mechanistic basis of PTEN-regulated GNMT expression, we employed genetic and pharmacological modulation in PC3 and LNCaP prostate cancer cell lines that present a complete loss of PTEN. In order to ascertain which components of this pathway are needed for the regulation of GNMT, we inhibited various proximal and distal effectors of PI3K, using BKM120 (BKM, Pan-PI3K inhibitor), MK2206 (MK, AKT inhibitor), and Rapamycin (R, mTOR complex 1 -mTORC1- inhibitor) (Supplementary Fig. S1A, B) [9]. This evidence concerns the gene PTEN and prostate carcinoma.