AP1S3 has not been shown to have any association with plaque psoriasis, though findings have shown that loss of function mutations in AP1S3 increases the risk of pustular psoriasis independent of CARD14 and IL36RN, with Mahil et al. showing that knock out of the gene causes autophagy in keratinocytes, mediating NF-κB activation [17]. Here, AP1S3 is linked to psoriasis vulgaris.