Endometriosis (EMS) is a chronic, estrogen-dependent inflammatory disease characterized by growth of endometrial tissue outside the uterine cavity. Symptoms in EMS patients include severe pelvic pain, dysmenorrhea, dyspareunia and infertility. To date, medical therapies are mostly based on hormonal suppressive drugs that induce a hypoestrogenic state. Although being effective regarding the reduction of endometriotic tissue masses and pelvic pain, this treatment is accompanied by severe side effects. Since EMS is associated with chronic inflammation, novel therapeutic strategies also focus on immune modulating drugs. However, little is known about how and to what extent immune cell subsets contribute to the network of locally produced cytokines, chemokines and other mitogenic factors that modulate the growth of ectopic endometrial implants and the inflammation associated with them. Mast cells (MCs) are known to be key players of the immune system, especially during allergic reactions. However, in recent years MCs have been identified to exhibit a far broader range of functions and to be involved in host defense and wound healing responses. Here, recent reports that imply an involvement of MCs in EMS has been reviewed, while the value of novel mouse models for clarifying their contribution to the pathology of this condition has been discussed.