Thus, OPCML operates extracellularly as a GPI-anchored protein and its post-translational mechanism is clearly distinct from that of other defined tumor suppressors, including genes that function through transcriptional repression (e.g., TP53), chromatin remodelling (e.g., ARID1A), or the cytoplasmic protein PTEN which regulates AKT signaling. This evidence concerns the gene AKT1 and neoplasm.