For example, in the case of the association of low FCGR3B copy number with systemic lupus erythematosus (SLE), it is the presence of a zero-copy FCGR3B haplotype, which leads to aberrant expression of a chimeric gene, FCGR2B’, in natural killer cells, that may be the key factor in an increased SLE risk, and not a reduced dosage of FCGR3B[13, 14]. This evidence concerns the gene FCGR2B and systemic lupus erythematosus.