Comparison of CCR6+IMQ with CCR6–IMQ subsets revealed eukaryotic translation elongation, eukaryotic translation termination, response of EIF2AK4 (GCN2) to amino acid deficiency, SRP-dependent cotranslational protein targeting to membrane, eukaryotic translation initiation, nonsense-mediated decay, selenoamino acid metabolism, EIF2 signaling, and major pathway of rRNA processing in the nucleolus and cytosol as the significantly upregulated pathways of CCR6+IMQ subsets in psoriasis when compared with CCR6–IMQ subsets in psoriasis (Fig. 3A). The gene discussed is UCN2; the disease is psoriasis.