TYK2 inhibition with deucravacitinib is mechanistically attractive because TYK2 lies upstream of both IL-23 and type I interferon signaling; early trials and translational studies suggest improvement in CLE molecular signatures and SLE activity [35,36,37], and isolated real-world reports describe concurrent control of psoriasis, PsA, and SLE [35]. The gene discussed is TYK2; the disease is psoriasis.