Genetic variations in 
CRISPR/Cas9 was used to generate human U937 monocytes with A20 DUB-inactivating 
Genetic disruption of A20 DUB domain in human and murine myeloid cells did not give rise to enhanced NF-κB signalling. Instead, cells with 
We propose that genetic alterations disrupting the A20 DUB domain mediate increased susceptibility to SLE through the upregulation of 