Several cytokines and chemokines have been shown to be deregulated in wAIHA.24 In our study, the different expression of cytokine genes across AIHA disease phases further support the contribution of T-cells and monocytes to the pro-inflammatory bone marrow milieu.21,25,26 At relapse, TNF-alpha and its superfamily genes, IL-1, IL-6, IL-17, IL-27 were upregulated in both CD4+ memory and in CD8+ effectors and memory cells. This evidence concerns the gene IL17A and autoimmune hemolytic anemia.