Another study demonstrated that KRAS mutations could induce the upregulation of PD-L1 expression through p-ERK but not p-AKT signaling, which mediates immune escape of human lung adenocarcinoma (LUAD), and thus blockade of the PD-1/PD-L1 pathway could reverse T-cell apoptosis to promote antitumor effect in a coculture system (63). Here, CD274 is linked to lung adenocarcinoma.