Consequence of hypoxia/reoxygenation phenomena, a characteristic aspect of OSA, is the activation of NF-kB and increased production of inflammatory cytokines [15] and the differentiation of Th17 cells [16] that are characterized by the expression of retinoic acid-receptor (RAR)-related orphan receptor (ROR)γt transcription factor, encoded by gene RORc [17] and by the production of IL-17, a cytokine that play a critical role in inflammatory, autoimmune and infectious diseases. Here, NFKB1 is linked to infectious disease.