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Kéfer et al. describe a compelling case in which chronic Angiostrongylus vasorum infection produced a restricted gammopathy pattern resembling a monoclonal process [1]. This observation is noteworthy because it challenges the traditional teaching that gammopathies in parasitic diseases are broadly polyclonal. We would like to expand on three aspects of this report that carry broader implications for veterinary clinical pathology. First, diagnostic interpretation. A narrow-based gamma peak on electrophoresis often raises alarm for neoplasia. Yet, as demonstrated here, chronic antigenic stimulation can generate oligoclonal expansions nearly indistinguishable from monoclonal profiles. Recent analyses in dogs with vector-borne diseases confirm that up to one-third of “suspicious” electrophoretic profiles revert to polyclonal when immunofixation is applied [2-4]. Moreover, a previous study already documented a characteristic beta-2 fraction peak in naturally infected dogs with A. vasorum [5], suggesting that this parasite is capable of inducing distinctive but variable electrophoretic abnormalities. Together, these findings underscore that electrophoresis alone risks overestimating monoclonal gammopathy prevalence in infectious contexts. Second, the immunopathogenic mechanism. Prolonged A. vasorum infection may create sustained B-cell stimulation akin to that described in canine leishmaniasis and ehrlichiosis, where chronic antigen exposure drives limited plasma cell clone expansion [6, 7]. One intriguing hypothesis is that lungworm antigens exert selective pressure on specific B-cell repertoires, producing restricted antibody populations that appear monoclonal in capillary zone electrophoresis. Testing this hypothesis will require integration of immunophenotyping and immunoglobulin gene sequencing in future cases. Third, clinical management. The rapid normalization of both hyperglobulinemia and proteinuria after anthelmintic therapy strongly supports a reactive process rather than underlying neoplasia. This case illustrates the importance of repeating electrophoresis posttreatment before subjecting patients to invasive diagnostics such as bone marrow aspiration. From a clinical pathology standpoint, this approach not only prevents misclassification but also reduces patient risk and healthcare costs. Going forward, prospective studies of dogs with chronic angiostrongylosis should incorporate electrophoresis, immunofixation, and molecular B-cell assays. Such work could clarify whether restricted gammopathies are rare curiosities or under-recognized consequences of chronic helminth infection. Kéfer et al.'s case provides a crucial stimulus for this line of inquiry, and we commend them for bringing attention to an overlooked facet of lungworm pathophysiology. The authors declare no conflicts of interest.