Similarly, somatic deletions within the PRKN gene sequence could potentially disrupt the regulatory sequences and tissue-specific enhancers acting on QKI gene expression, leading to an underestimation of QKI alterations in GBM while overestimating the tumor suppressor function of PRKN. Mapping of long-range chromatin interactions and identification of putative regulatory regions within Ch6q using functional and genetic assays will provide critical insights on this matter. Here, PRKN is linked to glioblastoma.