The snail Biomphalaria glabrata kills the blood fluke Schistosoma mansoni by a mechanism involving production of hydrogen peroxide, the enzymatic product of cytosolic Cu/Zn superoxide dismutase (SOD1). This enzyme exhibits higher activity in blood cells (hemocytes) from a predominantly resistant strain of B. glabrata than in hemocytes from a susceptible strain. Additionally, B. glabrata SOD1 polymorphisms have been associated with susceptibility/resistance to the parasite. To address the hypothesis that SOD1 transcription levels differ in accordance with variation at the SOD1 locus, quantitative PCR was performed using hemocyte-derived cDNA prepared from SOD1-genotyped snails. Here we report that individuals possessing the allele previously associated with resistance to S. mansoni express significantly higher levels of hemocyte SOD1 transcripts than individuals lacking this allele. A causal relationship between SOD1 expression and susceptibility/resistance to S. mansoni is supported by the correlation of transcript quantity with data (from a previous study) on the probability of infection.