Using the PLD inhibitor FIPI that blocks the enzymatic activity of both isoforms PLD1 and PLD2 revealed that PLD1-mediated regulation of TNF-α, cardiac function and scar formation is dependent on the non-enzymatic properties of PLD, while the migration of inflammatory cells into the infarct border zone after MI depends on the lipase activity of PLD. This evidence concerns the gene PLD2 and myocardial infarction.