In animals with a normal germline, ER stress induces germ cell apoptosis. Inactivation of the gld-1 genes alters many aspects of germ cell fate: differentiation of germ cells into oocytes is abrogated, germ cell proliferation is enhanced, a germline tumor is formed and the germ cells lose their responsiveness to execute physiological and stress-induced apoptosis. Furthermore, in gld-1 deficient animals the germ cells are prone to generate teratoma as they become sensitized to precociously transdifferentiate into somatic cells. Under these conditions ER stress can suppress and limit the germline tumor. This suppression is achieved by enhancing germline transdifferentiation into ectopic somatic cells. Soon after the transdifferentiation, these ectopic cells undergo apoptosis, and are removed from the gonad, suppressing the germline tumor.