Neuroinflammation has been related to models of surgery-induced cognitive dysfunction, in particular, the release of pro-inflammatory cytokines as tumor necrosis factor-alpha (TNF-α) and interleukin-1 beta (IL-1β) and the activation of nuclear factor-kB (NF-kB) signaling in macrophages and microglia have been highlighted as critical factors in the development of cognitive deficits [7–9]. Here, IL1B is linked to Cognitive impairment.