Brain ventricles (fluid-filled cavities formed from the lumen of the neural tube) are essential for normal vertebrate brain function. Jennifer Gutzman and Hazel Sive now uncover a role for the myosin phosphatase inhibitory regulator mypt1 in the expansion of the hindbrain ventricle in zebrafish embryos (see p. 795). Myosin phosphatase regulates non-muscle myosin II contractility by regulating the phosphorylation of the myosin regulatory light chain (MRLC). The researchers report that a mutation in mypt1 produces a small hindbrain ventricle and disrupts the morphogenesis of the hindbrain rhombomeres (structures that differentiate into specific cranial nerves). In addition, although MRLC phosphorylation levels change during hindbrain morphogenesis in wild-type zebrafish embryos, they are consistently high in mypt1 mutants, and inhibition of myosin II function rescues all of the defects observed in mypt1 mutants. The researchers suggest, therefore, that myosin phosphatase activity `relaxes' the neuroepithelium by reducing myosin contractility, thereby facilitating hindbrain morphogenesis and ventricle expansion. Epithelial relaxation, they add, might also facilitate tube inflation in other organs.