Recently, researchers reported that silencing cyclin L1 (CCNL1) via AAV9-cTnT-CCNL1 shRNA enhances the percentage of Ki67-positive and phospho-histone H3 (pHH3)-positive cardiomyocytes in MI mice, thereby promoting cardiac repair within the infarct zone and improving cardiac function [56]. Here, CCNL1 is linked to myocardial infarction.