Numerous genes derived from retroviruses are known to be expressed in mammalian genital tracts, particularly the uterus and placenta. Syncytin 1 and 2 in humans and syncytin A and B in mice are membrane proteins originating from envelope genes of endogenous retroviruses (ERVs), and are involved in the fusion of trophoblast cells, resulting in multinucleated syncytiotrophoblast formation. Recent studies have shown that syncytin-like putative fusogenic proteins are expressed in the placenta of rabbits and possibly cows. Today, it is believed that ERVs play an important role in trophoblast development and placental formation. However, the syncytin genes so far characterized have been endogenized to the host genome only within the past 12–40 million years, more recently than the acquisition of mammalian placenta, estimated to be more than 100 million years ago. This time difference has not been explained. In this review, we present these ERVs and related but distinct fusogenic and non-fusogenic genes, and discuss their potential roles in placental development. We then propose our “baton pass” hypothesis, in which a new gene such as one of the ERVs replaced a pre-existing gene and acquired the role that gene had played, accounting for time differences between ERVs endogenization and placental evolution.