Analysis in this way showed that the mutant construct increased NF-κB activity to a considerably higher level than the wild-type construct in MCF-7, WM266-4, and WM1552C cells, consistent with a role for this variant in driving tumor growth through the NF-κB pathway, akin to mutation of CYLD. To further confirm that the p.V1092A ALPK1 mutation activates NF-κB signaling, we performed immunohistochemistry and found that p65 staining of ALPK1 mutant spiradenomas was indistinguishable from staining of CYLD mutant cylindromas (Fig. 4c). The gene discussed is NFKB1; the disease is benign spiradenoma.