Warfarin resistance associated with continuous enteral ube feedings was first reported in the early 1980s [1–5]. his resistance was originally attributed to the large mounts of vitamin K contained within the feedings. In the arly 1980s, patients often received as much as 1500 to 000 g of vitamin K per day or more [1–5]. Industry esponded to this significant drug–enteral feeding interacion by markedly decreasing the amount of vitamin K in heir liquid enteral feeding formulations (Table 1). Howver, despite this massive reduction in vitamin K content, I ave observed problems of achieving therapeutic anticoaglation when warfarin is given concomitantly with continous liquid enteral feeding or significant increases in the nternational normalized ratio (INR) for prothrombin time ithout a change in warfarin dosage when the enteral feedng is discontinued. The intent of this column is to discuss lausible “new” evidence-based explanations for this “old” rug–enteral tube feeding interaction.