Blake’s pouch is a normal, transient embryologic cysticappearing structure that represents posterior ballooning of the inferior medullary velum into the cisterna magna, below and posterior to the vermis that communicates with open fourth ventricle through foramen of Magendie. Blake’s pouch cyst is caused by a failure of regression of Blake’s pouch secondary to the nonperforation of the foramen of Magendie.1–3 Importantly, during embryologic development, the foramina of Luschka open later4 than the foramen of Magendie.5–7 Therefore, in case of nonperforation of the foramen of Magendie, the fourth ventricle will enlarge together with the supratentorial ventricles until the foramina of Luschka open and establish an equilibrium of cerebrospinal fluid (CSF) outflow from the ventricles into the cisterns.8 However, as the larger foramen of Magendie is permanently missing, the ventricles may stay enlarged (►Fig. 1). According to this theory, in case of Blake’s pouch cyst, the cerebellar hemispheres and vermis would rather be compressed (to a certain degree) (►Fig. 2) than underdeveloped, and would therefore reexpand in case of ventricular shunting.9 Only one case Blake’s pouch cyst has been reported from India by Vakakmudi et al, except for a case in utero, in which a diagnosis of Blake’s pouch cyst was made on prenatal ultrasound and later confirmed by magnetic resonance imaging (MRI). Differentiating Blake’s pouch cyst from other posterior fossa cysts and cyst-like malformations and recognizing the accompanying hydrocephalus that are essentially noncommunicating have important implications not only on clinical management but also on genetic counseling, which is unnecessary in case of Blake’s pouch cyst.