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Red blood cell dysfunction is linked to overnutrition, which is characterized by inflammation, platelet aggregation and hypercoagulability. Although the role of MAPK in platelets is well established, little is known about the connection between MKPs and red blood cell. We investigated the pathophysiological effects of MKP-2 deletion on bleeding tendencies in platelet counts, and red blood cell indices that are brought on by high-fat diet. In this study, we demonstrated that female Mkp-2^-/- mice bleeding times were significantly shortened when they were fed chow diet. Male Mkp-2^-/- mice on a high-fat diet show resistance to diet-obesity, which is linked to a shorter bleeding time. In high-fat diet-fed male Mkp-2^-/- mice, we observed decreased levels of red blood cells, hemoglobin, and hematocrit. These data suggest that the anemia in these mice may be due to inflammation induced by obesity. When male Mkp-2^-/- mice were compared to wild-type controls, their platelet counts were normal; however, the platelets derived from these mice showed increased activation of p38 MAPK and ERK and SDF-1 expression. All of these studies point to a new function for MKP-2 in red blood cell physiology and hemostasis, which may have consequences for thrombotic and hemostatic diseases.