Some empirical evidence helps confirm this, as follows: (1) When performing knockdown of WISPER with GapmeR, post-MI mice have smaller infarct sizes, reduce fibrosis, and preserve cardiac structure and function; (2) WISPER directly interacts with TIAR (TIA1-related) to regulate the alternative splicing of PLOD2 (procollagen-lysine, 2-oxoglutarate 5-dioxygenase 2), which catalyzes cross-linking lysyl hydroxylation reactions and collagen deposition [44] (3) Knockdown Wisper blocks transmembrane shuttling of TIAR protein to the nucleus and prevents TIAR-PLOD2 interaction. The gene discussed is TIAL1; the disease is myocardial infarction.