As aforementioned, these treatment-resistant lesions are genomically characterized by biallelic PTEN loss and upregulation of VEGFA; taken together, these data indicate that PTEN loss promotes an immunologically excluded tumor microenvironment through upregulation of inhibitory cytokines and downregulation of PD-1, suggesting that PTEN significantly mediates acquired resistance to ICB monotherapy [62]. The gene discussed is PTEN; the disease is neoplasm.