Although the molecular mechanisms that mediate this process still need more clarifications, some observations indicate the: (i) the defective clearance of apoptotic bodies [43] and their impaired phagocytosis by macrophages [44]; (ii) neutrophils extracellular traps (NETs) as an additional source of nucleic acids [45]; and (iii) the overexpression of TLR7 (in lupus prone (BXSB) and transgenic mice (Y chromosome autoimmune accelerator, Yaa and Tlr7 duplication)), that drives the proliferation and differentiation of B cells leading to an increased production of antibodies [46,47]. Here, TLR7 is linked to systemic lupus erythematosus.