In combined FV and FVIII deficiency, our knowledge about the clinical manifestation so far is based on just one or two large series published in the literature. There is a need for careful documentation of clinical data from different population to see what the profile is for large number of patients and whether there are any ethnic differences. Further molecular studies to identify the causative mutations in patients with this disease will shed light on the basis for the clinical diversity seen among the patients. We studied CD1d-restricted invariant natural killer T (iNKT) cells in classical Hodgkin lymphoma (cHL). Tumor cells stained positive for CD1d in 21/44 cHL cases, whereas in non-Hodgkin lymphoma (NHL), only 9/31 stained positive. In contrast, CD1c expression was more common in NHL. The percentage of iNKT cells in cHL cell suspensions was similar to the percentage in reactive lymph nodes and was not related to the CD1d expression status of the tumor cells. In conclusion, we found expression of CD1d in HRS cells in half of the cHL cases, and also observed a substantial population of iNKT cells in cHL cell suspensions. Classical Hodgkin lymphoma (cHL) is a B-cell neoplasm characterized by a minority of neoplastic cells, the Hodgkin and Reed-Sternberg (HRS) cells, which are located within an extensive infiltrate of reactive cells, such as T cells, B cells, plasma cells, stromal cells, eosinophils, and macrophages. The HRS cells shape their microenvironment by attracting specific favorable T cell subsets, like regulatory T (Treg) and T helper 2 (TH-2) cells and producing factors such as CC-chemokine ligand 17 (CCL17 or TARC), transforming growth factor (TGF)-b and interleukin (IL)-10 [1] . Additionally, HLA class I is downregulated in HRS cells in 65% of the cHL cases and HLA class II in 40%, possibly as a strategy to escape from an effective immune surveillance [2] . All together, these factors may suppress the development of an effective antitumor response and provide a microenvironment that is favorable for the HRS cells.