Mechanical trauma during hemodialyses and heart‐lung bypass can result in shortened red cell life span. The nature of the membrane defect caused by these subhemolytic stresses is not known. The recent literature on the roles of ATP,Ca++,and membrane proteins in erythrocyte deformability is reviewed. New results by the luciferin‐luciferase assay show ATP levels as a function of subhemolytic shear stress for 2‐min exposure, and how ATP levels of normal cells vary when incubated in adenosine or 2‐deoxyglucose. The decrease in cell deformability accompanying mechanical trauma was measured by the increased pressure drop required for the cells to traverse the 3‐μm pores of a Nuclepore filter at a constant volumetric flow rate. Finally, a possible explanation for the observed partial recovery of deformability following adenosine incubation is presented.