The interaction between α-MHC and Titin is essential for maintaining myosin stability under physiological conditions, and this interaction is reduced during heart failure.6 To test if the α-MHC K1897 lactylation plays a role in facilitating binding to Titin, we assessed the effects of K1897, K1533, and K1249 residues on the interaction between α-MHC and Titin under physiological and Ang II-treated conditions. This evidence concerns the gene TTN and heart failure.