In psoriasis, MIR31HG was found to be elevated in psoriasis lesions and the upregulation of MIR31HG required IL-17A, IL-22, TNF-α, and IL-1α stimulation, demonstrating that nuclear factor kappa B inhibitor (NF-κB) signalling could be crucial crosstalk in psoriasis. Here, IL1A is linked to psoriasis.