Because Rap1a and Rap1b may have redundant functions (Table1), to fully evaluate Rap1 functions and avoid obvious early developmental defects, we injected embryos with MO oligonucleotides each at 2.5 ng/nl, and observed constant defects, i.e., over 90% of double rap1 knock-down morphants showed heart, trunk and caudal fin-fold phenotypes but intracranial hemorrhage remains a specific phenotype caused by rap1bMO (Fig. 1C, and Table1). The gene discussed is RAP1B; the disease is intracranial hemorrhage.