Cells from cluster 1 (KRT6A/B/C, S100A7, S100A8, S100A9) were specifically enriched in pathways such as necroptosis, eicosanoid signaling, and IL-17 signaling in psoriasis, in line with the MF8 histological pattern of psoriasiform epidermal hyperplasia, whereas cells from cluster 4 (IFITM1, PDPN, WNT10A, IGFBP3) upregulated the IFN, estrogen, and integrin signaling cascades (Figure 4, E and F). This evidence concerns the gene S100A9 and hyperplasia.