STARD13/DLC2 encodes a Rho GTPase activating protein and was identified from a region of chromosome 13 exhibiting a loss of heterozygosity in hepatocellular carcinoma [52]. It is a tumor suppressor that antagonizes Rho expression [53], and its downregulation or deletion has been reported in multiple cancers [54,55]. Supporting its role as a regulator of IFNβ-induced genes, an intronic SNP in STARD13 was amongst eighteen that were replicated in a study of responders to IFNβ therapy in MS patients [56]. Further, SNPs in OAS1 have been associated with MS susceptibility [57]. Therefore, this particular gene cluster and its predicted regulatory partner, STARD13, may be interacting determinants of the response to various negative stimuli. This also proposes the hypothesis that the role of STARD13 as a tumor suppressor is from its induction in response to DNA damage, and that deletion of this region in at least ten different cancers is pathogenic possibly due to hyper-activation of Rho, which promotes migration, proliferation, and invasion [58]. In this case, beyond improvement of the total lack of significant association from the individual eQTLs, creQTL proposed a more complete picture of the biological pathway.
