Beyond the NF-κB pathway, NGS studies have identified other recurrently altered signaling pathways in CTCL patients which may play a role in CTCL pathogenesis, such as JAK–STAT, PI3K-serine/threonine protein kinases, fibroblast growth factor receptors, and peroxisome proliferator-activated receptors (124). The gene discussed is SOAT1; the disease is primary cutaneous T-cell non-Hodgkin lymphoma.