Inhibition of the PD‐1/PD‐L1 axis restores T‐cell exhaustion and eradicates tumor cells.[13] The interferon (IFN)‐γ/Janus kinase (JAK)/signal transducer and activator of transcription (STAT) signaling pathway, which is induced by extracellular IFN‐γ, has been widely recognized as the predominant inducer of PD‐L1.[13, 14, 15] After IFN‐γ binds to its receptor, trans‐activated JAKs (JAK1 and JAK2) promote tyrosine phosphorylation of STATs (mainly STAT1). The gene discussed is PDCD1; the disease is neoplasm.