GENES IN LUPUS

TREX1" the major 3'->5' DNA exonuclease in human cells. The protein is a non-processive exonuclease that may serve a proofreading function for a human DNA polymerase. It is also a component of the SET complex, and acts to rapidly degrade 3' ends of nicked DNA during granzyme A-mediated cell death. Mutations in this gene result in Aicardi-Goutieres syndrome, chilblain lupus, RVCL (Retinal Vasculopathy with Cerebral Leukodystrophy), and Cree encephalitis. Multiple transcript variants encoding different isoforms have been found for this gene.<sup>[4]wikipedia"

This explanation have 3 fundamental points that underlie auto-immune disease  
deficiency is 
1. genetic based
2. Involve degradation and disposing of debris
3. Heterogeneity is a strong variable
but it also points to 2 additional facts pattern of Methylation which by now we know to be strongly influenced Estrogen will mark significant difference in expression of this disease in the 2 sexes!</sup>

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BANK1
It is involved in B-cell receptor induced Ca2+ mobilization from intracellular stores and promotes Lyn-mediated phosphorylation of IP3 receptors 1 and 2.. Lyn has emerged as a key enzyme involved in the regulation of cell activation. In these cells, a small amount of LYN is associated with cell surface receptor proteins, including the B cell antigen receptor (BCR),^[5][6] CD40,^[7] or CD19.^[8]..
Lyn has been described to have an inhibitory role in myeloid lineage proliferation.^[9] Following engagement of the B cell receptors, Lyn undergoes rapid phosphorylation and activation. LYN activation triggers a cascade of signaling events mediated by Lyn phosphorylation of tyrosine residues within the immunoreceptor tyrosine-based activation motifs (ITAM) of the receptor proteins, and subsequent recruitment and activation of other kinases including Syk, phosholipase Cγ2 (PLCγ2) and phosphatidyl inositol-3 kinase.^[8][10] These kinases provide activation signals, which play critical roles in proliferation, Ca²⁺ mobilization and cell differentiation. Lyn plays an essential role in the transmission of inhibitory signals through phosphorylation of tyrosine residues within the immunoreceptor tyrosine-based inhibitory motifs (ITIM) in regulatory proteins such as CD22, PIR-B and FCγRIIb1. Their ITIM phosphorylation subsequently leads to recruitment and activation of phosphatases such as SHIP-1 and SHP-1,^{[11][12][13][14][15]} which further downmodulate signaling pathways, attenuate cell activation and can mediate tolerance. In B cells, Lyn sets the threshold of cell signaling and maintains the balance between activation and inhibition. Lyn thus functions as a rheostat that modulates signaling rather than as a binary on-off switch.^[16][17][18]
Lyn has also been implicated to have a role in the insulin signaling pathway. Activated Lyn phosphorylates insulin receptor substrate 1 (IRS1). This phosphorylation of IRS1 leads to an increase in translocation of Glut-4 to the cell membrane and increased glucose utilization.^[19] In turn, activation of the insulin receptor has been shown to increase autophosphorylation of Lyn suggesting a possible feedback loop.^[20] The insulin secretagogue, glimepiride (Amaryl®) activates Lyn in adipocytes via the disruption of lipid rafts.^[21] This indirect Lyn activation may modulate the extrapancreatic glycemic control activity of glimepiride.^{[21][22]wikipedia} "

TNFSF4, a member of the dangerous Tumor Necrosis Factor family,  TNF is bad because its devastating effect escape mitigation by steroids and Interferon gamma at certain thresholds!
direct involvement with Death receptors are to be feared!

BLK
TNFAIP3
C2
C1QA
STAT4
PTPN22
LYN
IRAK1
ITGAM
IRFS
C4A,B
CRP
DRB1 1501
 DRB1 0301
FCGR2A, 3A