Exon 2, which encodes the first transmembrane domain, was replaced with a neomycin resistance gene. Sequenc analysis of a transcript present in mutant mice showed that exon 1 had spliced to exon 3 causing a frameshift mutation that introduced a stop codon in exon 3. While a cytoplasmic domain may have been produced, flow cytometric analysis of bone marrow macrophages showed no cell surface protein expression.