Previous research by Raba and Tabarkiewicz showed a correlation between the level of cytokines influencing PTB [28], and multiple authors described the effect of CBR2 stimulation on the release of cytokines. Moreover, the CBR may be stimulated by several cytokines (IL-1, IL-4, IL-10, IL-6, TNF-a, IL-8, MIP-1 (CCL3 and CCL4), RANTES (CCL5)) [29–31]. This interplay suggests a complex relationship between cytokine activity and CBR function, and further studies are needed to establish the correlation between specific cytokines and CBR2 stimulation in pregnant women. An algorithm based on the measurement of the concentration of specific cytokines might help predict PTB [28]. The ECS modulates the action of leukocytes by stimulating the CBR2 presented on the leukocyte cells [32], which then inhibit the inflammatory response [33,34]. This mechanism was observed in utero in patients with adenomyosis [35,36]. PTB might be associated with inflammation caused by an intraamniotic infection [37,38], but inflammation also plays a role in physiological term birth when no infection is present [34,39]. A decrease in the placental expression of the CBR2 might initiate inflammation, leading to a complete loss of the receptors [40].