Malignant Rhabdoid Tumors (MRT’s) are highly aggressive and often fatal pediatric tumors that can occur in the central nervous system (CNS) or outside the CNS. When they occur in the CNS, they are called atypical teratoid rhabdoid tumors (AT/RT) and are most common in children younger than 3 years of age. The loss of the tumor suppressor SMARCB1 on chromosome 22 as a result of homozygous deletions, truncating non-sense mutations or frameshift mutations is the common driver event in all MRT’s. SMARCB1 is a core component of the SWI/SNF chromatin-remodeling complex that regulates gene expression by reorganizing chromatin in an ATP dependent manner. Histopathologically, MRT’s are characterized by polyphenotypic differentiation. Since the SWI/SNF complex closely regulates differentiation, we examined the composition of the SWI/SNF complex in MRT’s derived from different locations using immunohistochemistry in a cohort of 43 rhabdoid tumors. Further, the expression of these SWI/SNF components during brain development was analyzed using gene expression data from the Allen Brain Atlas. We found that the expression of SMARCB1 was highest in the cerebellum throughout development. Global levels of other members of the SWI/SNF complex did not vary significantly during brain development. In MRTs, the expression of the core SWI/SNF members (SMARCC1, SMARCC2) remained relatively stable across tumors from different locations. Surprisingly, other SWI/SNF components including ARID1A, ARID1B and BRD7 show heterogeneity in expression depending on the location of tumors within the CNS. Other SWI/SNF members such as ACTL6A, ACTL6B, SMARCD1 and PBRM1 showed differences between the CNS and non-CNS tumors. These data have implications to understand the complex biology of MRTs.