Contrary to TNF-α contribution in the phenotypes related to cellular senescence and inflammaging where it reduced the activity of dermal fibroblasts, i.e., proliferation and collagen synthesis [13] as proven in our experiments (Figure 2c and Figure 3), the prolonged TNF-α presence in the epidermis results in the pathogenesis of autoimmune diseases such as psoriasis and psoriatic arthritis by activating keratinocytes and consequently promoting epidermal hyperplasia [52]. The gene discussed is TNF; the disease is psoriatic arthritis.