A prerequisite for the development of a malignant tumor is the occurrence of a series of mutations in suppressor genes, so that cells acquire a malignant phenotype. There is no single molecular alteration that would lead a cell through a complex process of carcinogenesis. In the case of late-stage ovarian cancer, the next necessary step is the escape of these genetically altered cells from the supervision of the host immune system. Initially, the process of evasion from immune control is merely one of “cheating” the immune system. However, as the tumor increases in size, it takes control over the immune system, at least on a local scale, and the escalation of this phenomenon may result in generalized immune suppression. First, a cancer cell masks its presence, then it inhibits the non-specific immune system as well as the specific immune response by (among other things) initiating the apoptosis of the cytotoxic cells infiltrating its microenvironment. Finally, cancer cells modify their microenvironment so that it supports their development and by accumulating immunosuppressive Treg lymphocytes inhibits the immune response against them. Understanding the principles governing this phenomenon would thus appear to be key to being able to, but also to counteract it. The resulting knowledge might allow us to supplement the standard combination of antitumor treatment and immune therapy, thus improving its efficacy. Currently one of the most promising forms of immune therapy is the removal of Treg cells from the tumor microenvironment.