STAT6 is required for IL-4-IL-13-dependent SOCS-1 expression in A549 human lung adenocarcinoma cells; three identified STAT6-binding motifs in the SOCS-1 promoter cooperate to induce maximal transcription.

Unphosphorylated STAT6 plays a novel role in the pathogenesis of non-small cell lung cancer.

Small interfering RNA against transcription factor STAT6 leads to increased cholesterol synthesis in lung cancer cell lines

tumors with the most common fusion variant, NAB2ex4-STAT6ex2/3, corresponded to classic pleuropulmonary solitary fibrous tumors with diffuse fibrosis and mostly benign behavior and occurred in older patients

Here, we demonstrate that pulmonary adenofibromas are neoplastic lesions harbouring NAB2-STAT6 fusion genes ,the molecular hallmark of solitary fibrous tumours.

ARHGAP24 inhibits cell proliferation and cell cycle progression and induces apoptosis of lung cancer via a STAT6-WWP2-p27 axis.

Activation of the IL-4/STAT6 Signaling pathway Promotes lung cancer Progression by Increasing M2 Myeloid Cells.