There were three studies that have demonstrated the correlation of leukocyte count with CAD incidence. Braunwald and colleagues evaluated the relationship between the PF-4217903 baseline white blood cell and angiographic findings as well as clinical outcomes in 2,208 patients with unstable angina/non-ST-segment elevation ACS. They found that elevated leukocytes count was not only associated with impaired epicardial and myocardial perfusion but also with the extent of CAD and higher mortality. Moreover, after adjustment for typical risk factors and other biomarkers, WBC count and hs-CRP could be used to stratify patients across an eightfold gradation of six-month mortality risk. Data from Rasouli M et al in a small sample size study on stable CAD suggested that the total leukocyte count and its subgroups were associated with the presence and severity of CAD, although this association was not independent from other coronary risk factors. Study performed by Avanzas et al. showed that neutrophil count and hs-CRP level were higher in patients of stable CAD compared to those without. Nevertheless, they detected that neutrophil count but not hs-CRP level was correlated with angiographic stenosis complexity. More recently, a prospective cohort study performed in 3005 patients with coronary angiography assessed the association of N/L ratio with the degree of CAD. They found that N/L ratio was qualified as an independently predictor for the extent of CAD and 3-years outcome using a multivariate regression analysis. Recently, clinical observations from Kaya and Sahin groups evaluated the severity of CAD using Syntax score and led to similar conclusion. Unfortunately, these studies did not focus on diabetic patients. Therefore, the present work not only confirmed findings of previous studies but also provided novel insights concerning the role of leukocytes and its subsets in predicting the presence and the extent of CAD in diabetic patients with stable angina pectoris. Additionally, our study determined the cut-off points of leukocytes and its subsets which can be most useful for predicting increased risk of severe CAD. Furthermore, we compared the relative predictive value of differential leukocyte counts and assessed which leukocyte subset was the most valuable marker for predicting the severity of CAD in patients with DM. Nonetheless, there are several limitations in our study. Firstly, the relatively small sample size from a single center study is a limitation. Secondly, we did not combine leukocyte and its subsets count with other nonspecific inflammatory markers such as hsCRP, fibrinogen and HbA1c to increase the predictive ability due to the small sample size. Moreover, although leukocyte and the severity of CAD in diabetic patients in the present study are significantly associated, the power was relatively small, and we failed to evaluate the predictive power of other leukocyte subsets such as eosinophils and basophils. Finally, we did not evaluate the predictive value of leukocytes and its subsets in our population. Thus, the data should be replicated in a study with larger sample size and long term follow up.