The mechanism for ligand upregulation has been elucidated in part by Parsa et al., who found that loss of the phosphatase and tensin homolog (PTEN) led to increased PDL-1 gene transcription; furthermore, gliomas with wild-type PTEN were more likely to be lysed by tumor-specific T cells than gliomas with mutant or inactivated PTEN [68]. The gene discussed is PTEN; the disease is glioma.