The mechanism for this selection toward fetal rearrangements in B6.TC mice is unknown; however, it can be speculated that the Sle2c1 lupus susceptibility locus, which contains Ckdn2c and results in less p18 expression, could lead to a difference in expansion of B-1a cells with different BCR signaling requirements. This evidence concerns the gene BCR and systemic lupus erythematosus.