Indeed, lack of LKB1 has also been shown to induce accumulation of immunosuppressive adenosine in the TME, and a marked induction of HIF1A, endorsing the establishment of a “hypoxic” microenvironment in lung adenocarcinoma, characterized by a distinctive exclusion of T cells from TME and poor PD-L1 expression, defined as PD-L1-/TIL- type II cancer. This evidence concerns the gene HIF1A and lung adenocarcinoma.