Since an ESE can promote exon inclusion, mutation or deletion of the ESE would lead to less full-length but more truncated CD200. Our results showed that after mutating the ESE in exon 2, expression of full-length CD200 was reduced in both Daudi and SK-N cells. This expression pattern is the reverse of that seen for endogenous CD200 expression in SK-N cells, in which the predominant expression is of full-length CD200. To exclude the possibility that the mutation created a new exonic splicing silencer (ESS) which led to decreased full-length, and increased truncated CD200, we deleted the ESE and examined the changes in CD200:CD200 tr . Our result showed that deletion of the ESE promoted exon 2 exclusion, the same result as we obtained from mutation analysis, indicating that mutation of the ESE does not create an ESS.