Blood component transfusion is a life saving medical intervention. Prior to transfusion to patients, transfusion products such as red blood cells and platelets are stored within a blood bank. The quality of banked blood cells deteriorates during storage and can lead to adverse affects in patients post transfusion. The decline of red cell and platelet function during storage within a blood bank  is commonly referred to as storage lesion (SL) and is induced by multiple factors. One of these factors is metabolism. Metabolism changes during storage due to a combination of suboptimal storage conditions and intrinsic cellular programming. Our work on blood storage lesion aims to elucidate how red cell and platelet metabolism, under defined blood banking conditions as platelet and red cell concentrates, results in suboptimal red cell function and premature platelet activation. Subsequently, how may these be overcome?  Why are some patients more amenable to transfusion adverse effects than others? To answer these questions we are using a combination of mass spectrometry, hematological phenotyping and systems biochemistry methods.