TYK2 inhibition, changing treatment landscape for psoriasis.Psoriasis is a common immune-mediated inflammatory disease affecting approx. 2of individuals living in Western countries.The signaling of IL-23 is known to be transmitted through the Janus kinase (JAK)-signal transducer and activator of transcription (STAT) pathway.As TYK2 inhibitors are a relatively new treatment modality, there is not yet a com. available TYK2 inhibitor for clin. use.There are also other TYK2 inhibitors in development, such as brepocitinib (TYK2/JAK1) and PF-06826647 (TYK2/JAK2), but deucravacitinib is furthest in development and will be the focus of this editorial.Deucravacitinib is a novel, oral, selective TYK2 inhibitor with a unique mechanism of action through allosteric binding of the pseudokinase (JH2) domain which is regulatory in nature and lacks catalytic activity.Selective targeting of TYK2 results in the inhibition of signaling of IL-12, -23 and Type 1 IFN, the key cytokines involved in psoriasis pathogenesis.The overall place of deucravacitinib in the treatment of moderate-to-severe psoriasis involves multiple prescriber and patient factors, including safety, tolerability, efficacy, convenience, and impact on comorbidities.Deucravacitinib seems to check all the boxes.It has proven efficacy superior to apremilast in psoriasis, promising early phase results in psoriatic arthritis, and studies ongoing for inflammatory bowel disease.It is well tolerated with low rates of headache, nausea, and diarrhea and a favorable safety profile with low rates of AEs and no impact on laboratory parameters as seen with other JAK inhibitors.