Recent advances in skin omics suggest that increased cholesterol synthesis and downstream signaling may contribute to psoriasis through activation of proinflammatory pathways, including IL-17. The perspective proposes that UVB phototherapy may exert therapeutic effects not only through immunomodulation but also by reducing cholesterol synthesis and generating vitamin D, lumisterol, and tachysterol derivatives that act on nuclear receptors—particularly as inverse agonists of RORγ—thereby suppressing IL-17–driven inflammation. These mechanisms remain largely hypothetical but may inform future therapeutic strategies.