Although genetic drivers for tumorigenesis in FDC are largely unknown, recent genomic profiling studies have revealed several recurrent gene alterations in FDC sarcoma, including BRAF V600E mutation [15] and loss-of-function variants in tumor suppressor genes involved in the regulation of NF-κB pathway and cell cycle, such as NFKBIA, CYLD, CDKN2A, and RB1 genes [16]. The gene discussed is NFKBIA; the disease is sarcoma.