A possible explanation for this might be that: (1) increased lnc‐GAS5‐promoted apoptosis of vascular endothelial cells, resulting in arterial stenosis, which might play a role in the pathogenesis of AIS15, 18; (2) elevated lnc‐GAS5 could modulate enhancer of zeste homolog 2 (EZH2)‐mediated adenosine triphosphate‐binding cassette transporter A1 transcription to accelerate the progression of atherosclerosis, which might increase the risk of AIS15, 22; (3) lnc‐GAS5 might promote the formation of thrombosis, which could consequently accelerate AIS risk.4, 23. This evidence concerns the gene GAS5 and androgen insensitivity syndrome.