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On Sunday, 5 August 2012, at approximately 10:00 a.m., an armed Wade Michael Page walked into the Oak Creek, Wisconsin Sikh gurdwara, a place of worship. Page killed six worshippers and injured four others. Although the murderer had links to several white supremacist organizations, authorities would not speculate on the motive of this incident. In fact, the word race was rarely mentioned in relation to this case. The lack of a sustained examination of racism as a motivating factor in this crime was very troubling within the media's portrayal of this incident. Through a critical analysis of structural racism, this article highlights how the silences of racism, racialized identities, and the connections of racist acts such as the Wisconsin gurdwara murders to hate crimes perpetuates racialized and colonized violence on brown bodies. This structural racism absolves many Americans (and we would add many Canadians) of their deeply rooted racist beliefs and ideologies. By providing a counter-hegemonic narrative, this article discusses how the homogenization of brown bodies, such as Sikhs and Muslims, has very real material consequences in a North American context. Finally, this article discusses the problematic framing of this incident as "Domestic Terrorism" and the importance of de-Islamizing Sikhaphobia in the post-9-11-2001 context.

There are significant inter-individual differences in the levels of gene expression. Through modulation of gene expression, cis-acting variants represent an important source of phenotypic variation. Consequently, cis-regulatory SNPs associated with differential allelic expression are functional candidates for further investigation as disease-causing variants. To investigate whether common variants associated with differential allelic expression were involved in breast cancer susceptibility, a list of genes was established on the basis of their involvement in cancer related pathways and/or mechanisms. Thereafter, using data from a genome-wide map of allelic expression associated SNPs, 313 genetic variants were selected and their association with breast cancer risk was then evaluated in 46,451 breast cancer cases and 42,599 controls of European ancestry ascertained from 41 studies participating in the Breast Cancer Association Consortium. The associations were evaluated with overall breast cancer risk and with estrogen receptor negative and positive disease. One novel breast cancer susceptibility locus on 4q21 (rs11099601) was identified (OR = 1.05, P = 5.6x10-6). rs11099601 lies in a 135 kb linkage disequilibrium block containing several genes, including, HELQ, encoding the protein HEL308 a DNA dependant ATPase and DNA Helicase involved in DNA repair, MRPS18C encoding the Mitochondrial Ribosomal Protein S18C and FAM175A (ABRAXAS), encoding a BRCA1 BRCT domain-interacting protein involved in DNA damage response and double-strand break (DSB) repair. Expression QTL analysis in breast cancer tissue showed rs11099601 to be associated with HELQ (P = 8.28x10-14), MRPS18C (P = 1.94x10-27) and FAM175A (P = 3.83x10-3), explaining about 20%, 14% and 1%, respectively of the variance inexpression of these genes in breast carcinomas.