Vagaries of genetic association studies in myocardial infarction.

antineutrophil antibodies;7 and (2) tumor necrosis factor (TNF)– mediated myelosuppression, in a setting of rituximab-induced TNFrelease.8 Finally, detection of del(20)(q11.2) is evidence for secondary myelodysplastic syndrome related to high-dose therapy (HDT)9; nevertheless, as previously shown, one cannot exclude the possibility of stem cell damage resulting from prior conventional dose chemotherapy and actually unrelated to HDT.10