Deletion of GRP94/GP96 in different cells induce a hipoinflammatory and autoimmune state via instability in TLR and other molecules; in macrophages generate TLR null cells [45], in dendritic cell reduces the immune response to sepsis [52], while in Treg-cells, the levels of FOXP3 are reduced, inducing IFN-γ and IL-17 overproduction [53]. This evidence concerns the gene IL17A and Sepsis.