XRCC1 and Sepsis: Coincidentally, a recent study also confirmed that lactylation of XRCC1 leads to changes in its surface charge, thereby promoting its binding to importin‐α and ultimately resulting in the nuclear translocation of XRCC1.[63] Together, our findings suggest that H3K18la‐induced EGR1 expression and EGR1 lactylation are important mechanisms through which lactate promotes glycocalyx degradation via the activation of HPSE during sepsis.