The central area of these lesions frequently displays atrophy and hypopigmentation.[2] In DLE pathogenesis, type I and type II IFNs are pivotal, primarily through their activation of the JAK-STAT signaling pathway.[3] Conventional treatments for DLE involve topical agents, antimalarials, glucocorticoids, and immunosuppressants.[2]. Here, SOAT1 is linked to discoid lupus erythematosus.