Based on our findings, we hypothesize that during the progression of psoriasis, Th1 and Th17-derived cytokines (such as TNFα and IL17A) may induce PARP2 in keratinocytes, which may turn down aromatase activity and estrogen synthesis in keratinocytes that may trigger NF-κB activation. Here, NFKB1 is linked to psoriasis.