Recent work has identified two sub-pathways of NHEJ; classic and alternative (a.k.a., microhomology-mediated end-joining), with the latter involving a distinct set of proteins (e.g., PARP1, XRCC1, FEN1, MRE11, NBS1, LIG3, and POLθ), more commonly inducing extensive genomic alterations (typically deletions), and often being upregulated in cancer as a compensatory system [86]. This evidence concerns the gene MRE11 and cancer.