Critical mechanistic gaps persist: (1) The direct lactylation of RLF/SMCHD1 proteins necessitates validation through the use of site-specific antibodies, such as anti-RLF-Kla, in conjunction with mass spectrometry to accurately map the modification sites and assess their dynamics; (2) Temporal regulation of RLF/SMCHD1 across infarction phases (pro-inflammatory acute vs. pro-fibrotic repair) remains uncharacterized. Here, KL is linked to infarction.