In MS, POP-1 represses gut fate by preventing activation of end-1 and end-3, while in E, POP-1 is an activator that contributes to activation of end-1 through its association with a divergent β-catenin, SYS-1 (Maduro et al. 2005b; Shetty et al. 2005). The gene discussed is POP1; the disease is myeloid sarcoma.