Contrary to the evidence supporting the role for insulin in stimulating uterine contraction, only a limited number of studies have highlighted the inhibitory effect of insulin on myometrial contractions in human and rodent. A hypothetical narrative review of the current literature was conducted, revealing the current literature and shows the potential inhibitory effects of insulin on myometrial contractility. These inhibitory mechanisms include activation of adenylyl cyclase signaling pathways, an increase in cAMP production, a decrease in Ca2 + influx and cytosolic Ca2+, hyperpolarization of the cell membrane, and stimulation of NO synthesis. Altered oxytocin sensitivity, structural similarity to relaxin, modulating abscisic acid (ABA) effect, and synergistic interaction with progesterone, adiponectin, and leptin may also represent additional mechanisms for the inhibitory effects of insulin on myometrial contractions. The literature indicates that insulin exhibits inhibitory effects on myometrial contractility. Confirming such a conclusion through future studies may propose insulin as a possible uterine quiescent.