KT-474 is described as a first-in-class oral IRAK4 degrader. Can you explain how IRAK4 degradation differs from traditional kinase inhibition in blocking IL-1R/TLR signaling pathways?

 The interim Phase 2 data for KT-474 showed promising results in both hidradenitis suppurativa and atopic dermatitis. What specific clinical improvements were observed in patients with these conditions after 28 days of treatment?

KT-474 has been generally well-tolerated in clinical trials. Can you discuss any adverse events reported during the studies and how they compare to those seen with other anti-inflammatory therapies?

IRAK4 degradation by KT-474 resulted in a broad inhibition of TLR-mediated cytokine induction. How might this broad anti-inflammatory effect translate into clinical benefits across different inflammatory diseases?

Given the significant quality of life impacts of HS and AD, how did the reduction in symptoms like pain and pruritus affect the overall quality of life for patients in the KT-474 trials?

How does the efficacy of KT-474 in reducing inflammation and improving clinical symptoms compare to other existing treatments for HS and AD, such as biologics targeting TNF-α or IL-4/IL-13?

Kymera Therapeutics recently expanded the Phase 2 trials for KT-474. What are the objectives of this expansion, and what new data do you hope to gather from these larger patient cohorts?

Beyond HS and AD, KT-474 is being investigated for other immune-inflammatory diseases like rheumatoid arthritis. What potential does IRAK4 degradation have for treating these conditions, and what are the next steps in the clinical development of KT-474?