Programmed death-ligand 1 induced by tumor-associated macrophages promotes the progression of lung cancer through the JAK1/STAT3 signaling pathway, and the JAK1 inhibitor significantly improves the efficacy of anti-programmed cell death protein 1 immunotherapy in pancreatic cancer by inhibiting the activation of cytotoxic T lymphocytes [18, 19]. Here, JAK1 is linked to neoplasm.