Ficolin-3, encoded by the FCN3 gene and expressed in the lung and liver, is a 
recognition molecule in the lectin pathway of the complement system. 
Heterozygosity for an FCN3 frameshift mutation (rs28357092), leading to a 
distortion of the C-terminal end of the molecule, occurs in people without 
disease (allele frequency among whites, 0.01). We describe a patient with 
recurrent infections who was homozygous for this mutation, who had undetectable 
serum levels of ficolin-3, and who had a deficiency in ficolin-3-dependent 
complement activation.