From this, we conclude that the genetic basis of the tumor, i.e., Monosomy 3 with BAP1 loss, determines the primary upregulation of the NFkB pathway, which leads to an increase in HLA Class I expression in the tumor cells and production of cytokines and chemokines, which then attracts immune cells, further upregulating expression of HLA Class I. These data indicate that absence of the deubiquitinating function of BAP1 allows the NFkB pathway to be active, potentially by affecting the regulators of NFkB directly (Figure 4). This evidence concerns the gene NFKB1 and neoplasm.