Background TER119 is very widely used as a marker of the erythroid lineage in mice. It is variously regarded as a marker of a protein associated with Glycophorin A or specifically reacting with Glycophorin A itself. We previously reported a TER119-negative murine pedigree, derived by ENU-mutagenesis and recessive breeding, with a T>C variant at position 4634105 on chromosome 6 and exon 14 deletion (transmembrane region) in a sialyl-O-acetyl transferase, CASD1. Methods Glycophorin A and TER119 expression were evaluated by Western blot and flow cytometry. The blood picture for the TER-119neg pedigree was evaluated using standard techniques. CASD1 expression in erythroid precursors was measured by flow cytometry. Other changes in the profile of surface carbohydrates were evaluated by lectin binding. Results While a complete loss of the TER-119 epitope was confirmed by flow cytometry and immunoblot, normal levels of Glycophorin A were noted. There was no change in haematological parameters nor in osmotic fragility. Increased levels of wheat germ agglutinin binding were found in erythroid cells in CASD1-variant homozygotes. Levels of CASD1 expression decreased during erythroid differentiation. Discussion Through studies of a CASD1-variant pedigree, we determined that TER-119 is a sialyl epitope at least partially defined by a 9-O-acetyl sialic acid. The exact nature of the epitope defined by TER119 and any human equivalent remain to be determined.