“…The first step is to recognize the genes involved in AA, which seem to be inhibited during AA disease. In this disease, due to aggressive and aberrant immune responses of different subtypes of effector T cells (T effs ) and also tenuous regulatory T cells (T regs ) responses, it seems that development of AA is strongly associated with the low number and/or dysfunction of T regs alongside increase in aberrant immune responses, which have been recently discussed as the novel therapeutic options of AA Tavakolpour, 2016). Thus, we should seek for T regs -associated genes, like T regs transcription factor, forkhead box p3 (FOXP3) in addition to co-inhibitory molecules, including cytotoxic T-lymphocyteassociated protein 4 (CTLA-4), B-and T-lymphocyte attenuator (BTLA), programmed cell death protein 1 (PD-1), T-cell immunoglobulin, and mucin-domain containing-3 (TIM-3), CD160, lymphocyte activation gene-3 (LAG-3), and leukocyte-associated immunoglobulin-like receptor 1 (LAIR1).…”