Importantly, the pathogenesis of CTCL including SS is closely associated with chronic inflammation and aberrant activation of nuclear factor-κB (NF-κB) pathway, nuclear factor of activated T cells (NFAT) pathway, and Janus kinase / signal transducer of activation (Jak/STAT) pathway in lesional skin and blood [12–15]. Here, SOAT1 is linked to primary cutaneous T-cell non-Hodgkin lymphoma.