This explains why the homozygous VH10 heavy chain knock-in (which restricts its allelic exclusion during Igh VDJ recombination in pro-B cells) in our SWHEL mice, even without the Vκ10 light chain transgene, led to a notable reduction of B-1a cells, and a corresponding compounding effect on the B-1a lymphopenia in Dynll1 mutant animals (Fig 8B). Here, TNFSF14 is linked to lymphopenia.