BAFF is indispensable for B cell (especially the proatherogenic B2 subset) maturation and also aids the survival of low-affinity self-reactive B lymphocytes.101,103 Evidence reiterates that high circulating concentrations of BAFF and CCL7 in MI patients is associated with increased risk of mortality and recurrent infarction.101 An experimental study reported that deficiency of BAFF receptors resulted in significantly decreased levels of B2 cells but did not alter the number or function of the B1a (atheroprotective) subtype.103. This evidence concerns the gene TNFSF13B and myocardial infarction.