Several conclusions can be drawn from a review of the formation, function and regression of the corpus luteum. Ovulation and luteinization encompass degenerative and growth changes. Inflammatory conditions associated with ovulation lead to the breakdown of the follicle wall and the membrana granulosa, along with initial damage to theca and granulosa cells. The early corpus luteum is, therefore, a tissue in stress. Thus, one view of the corpus luteum is that it, like the phoenix, rises from the inflammatory ashes of the postovulatory follicle to exist briefly and to be consumed by a similar process at regression. The luteinization process is associated with parenchymal cell hypertrophy and matrix remodelling, which appear to be regulated by IGFs and androgens, and with angiogenesis, which is induced mostly by bFGF. High levels of functional activity of the corpus luteum are regulated by control at the level of the LH receptor, whose activation leads to the translocation of cholesterol into the cell and mitochondria for conversion to steroids. Functional luteal regression can be considered as another inflammatory-like condition with apparent activation of the immune system, along with cytokine, reactive oxygen, and eicosanoid production. Structural luteolysis is subsequently invoked that leads to matrix dissolution and cellular degeneration. It is perhaps not surprising that the invocation of immune activation, which causes the production of DNA-damaging reactive oxygen species and cytotoxic cytokines each cycle, may increase the risk of pathologies. One example may be ovarian cancer which appears to be associated with the use of fertility-enhancing drugs and associated with the number of ovulations in a woman's lifetime.