PAF is subsequently degraded by PAF acetylhydrolase (PAF-AH/Lp-PLA2). PAF-AH is classified into three types: intracellular PAF-AH I and PAF-AH II and extracellular plasma-type PAF-AH. Phospholipase A2 group VII (PLA2G7), encoded by the _PLA2G7_ gene, is a plasma-type PAF-AH that degrades PAF to biologically inactive products. In mice, PAF that is produced by macrophages and microglia activates the PAF on itself, robustly enhancing PAF production [15]. The increase in PAF production causes neuropathic pain through the PAF on primary sensory neurons, leading to the PAF-pain loop [15]. The PAF/PAFR system contributes to acute nociceptive and inflammatory pain, chronic pain (including neuropathic pain) [23; 24], inflammatory responses [25], mechanical allodynia, and hyperalgesia in animal models [17]. PAF also exacerbates nociceptive and inflammatory postoperative pain [26]. In humans, plasma PAF-AH activity decreased in patients with inflammatory conditions, such as active systemic lupus erythematosus, necrotizing enterocolitis [27], bronchial asthma [28], sepsis [29], and severe anaphylaxis [30], compared with healthy individuals, implying an increase in plasma PAF levels through a decrease in PAF-AH activity that may contribute to the pathogenesis of these inflammatory responses. For the association between PAF and pain, high plasma PAF levels correlated with the severity of menstrual pain in primary dysmenorrhea [31]. Notably, the activation of the PAFR amplifies pain in fibromyalgia, which has an element of neuropathic pain [32]. However, the direct association between plasma PAF-AH activity or plasma PAF concentrations and postoperative pain, including neuropathic pain, has not been reported in humans. The _PLA2G7_ gene is reportedly associated with cardiac disease and stroke [33], but there are no reports of an association with pain. The rs1051931 T/C single-nucleotide polymorphism (SNP) of the _PLA2G7_ gene leads to an amino acid substitution (Val379 Ala) of PLA2G7, and the PLA2G7 protein with Ala at 379 position was shown to result in a 2.7% decrease in PAF-AH activity in an aliquot of plasma in humans [34], although it is unclear whether the decrease in PAF-AH activity is attributable to a decrease in the PAF-AH enzymatic activity of PLA2G7 or a decrease in the mass of PLA2G7. Together with the facts that a decrease in plasma PAF-AH activity is related to inflammatory responses in humans [27; 28; 29], PAFR activation or high PAF levels are associated with menstrual pain in primary dysmenorrhea and fibromyalgia in humans [31; 32], and an increase in PAF production exacerbates postoperative pain (including neuropathic pain) in mice [15; 26], the decrease in PAF-AH activity in plasma caused by the _PLA2G7_ rs1051931 polymorphism may contribute to acute postoperative pain, including neuropathic pain, in humans through higher plasma levels of PAF. In the present study, we investigated the association between the rs1051931 polymorphism of the _PLA2G7_ gene, which decreases PAF-AH activity in plasma in humans, and dysesthesia after SSRO and pain severity after laparoscopic gynecologic surgery to clarify the association between PAF-AH activity and acute postoperative pain, including neuropathic pain-related dysesthesia, in humans.