BACKGROUND: Alopecia areata (AA) is an autoimmune disease resulting in hair loss 
with devastating psychosocial consequences. Despite its high prevalence, there 
are no FDA-approved treatments for AA. Prior studies have identified a prominent 
interferon signature in AA, which signals through JAK molecules.
METHODS: A patient with AA was enrolled in a clinical trial to examine the 
efficacy of baricitinib, a JAK1/2 inhibitor, to treat concomitant CANDLE 
syndrome. In vivo, preclinical studies were conducted using the C3H/HeJ AA mouse 
model to assess the mechanism of clinical improvement by baricitinib.
FINDINGS: The patient exhibited a striking improvement of his AA on baricitinib 
over several months. In vivo studies using the C3H/HeJ mouse model demonstrated 
a strong correlation between resolution of the interferon signature and clinical 
improvement during baricitinib treatment.
INTERPRETATION: Baricitinib may be an effective treatment for AA and warrants 
further investigation in clinical trials.