TLR4 and hydrops fetalis: HCK and IRF8 were identified to be important in predicting the occurrence of HF after MI.[26] Related studies have found that the upregulation of SPI1 expression during MI can aggravate cardiac tissue damage and disease progression by activating the TLR4/NF-κB axis.[27] Atherosclerosis is the main pathological basis of cardiovascular and cerebrovascular diseases.[28]LILRB3 is a reliable molecular biomarker for plaque status changes in stable coronary artery disease, ST-segment elevated MI progression, and MI recurrence.[29]