The mechanism of interferon signaling in response to 8–MOP + UVA, including the dependence of the STING transcriptional signature on IFN receptors and on the signaling cascade downstream from the receptors (JAK/STAT), should be carefully evaluated in CTCL cell lines and, if technically feasible, in patient-derived CTCL cells. The gene discussed is SOAT1; the disease is primary cutaneous T-cell non-Hodgkin lymphoma.