Jialin Wang’s team discovered that YB-1 in IRI environments not only activates NET formation but also functions as a critical non-specific component enabling NETs to attack renal tubular cells, and through blockade of YB-1-mediated NET-related inflammatory cascades using a YB-1 antibody, they attenuated AKI progression, thereby proposing YB-1 as a novel therapeutic target for AKI (11). The gene discussed is YBX1; the disease is acute kidney injury.