JAK2‐STAT1 activation contributes to IFNγ antiproliferative effect while PI3K‐ACT activation induces PD‐L1 expression and decreases IFNγ antiproliferative effect, implying that blockade of PI3K might maximize the IFNγ mediated antitumor effect.16 These findings indicate a crosstalk between JAK2‐STAT1 and PI3K‐AKT pathways in response to IFNγ in lung adenocarcinoma. The gene discussed is AKT1; the disease is lung adenocarcinoma.