We learn with curiosity the current research by Benezeder et al,1 which recognized transcriptomic convergence between acute generalized exanthematous pustulosis (AGEP) and generalized pustular psoriasis (GPP), significantly by way of IL-36–pushed inflammatory pathways. Though these findings provide worthwhile perception into shared effector mechanisms, we warning towards, at this stage, decoding transcriptomic similarity as proof for illness id, particularly when the medical course and immune activation pathways diverge.
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