To date, most studies have explored the intrinsic molecular features of SS, demonstrating that it is characterized by a complex profile of chromosome aberrations [7,8,9] and a broad range of genes variously affected by somatic copy-number alterations and somatic single-nucleotide variants that are involved predominantly in T-cell activation and apoptosis, activation of NF-kB, JAK/STAT signaling, chromatin remodeling, and DNA damage response [10,11]. The gene discussed is NFKB1; the disease is synovial sarcoma.