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Zhao Tian*, Tang Zhiping�� Zhang Xibao. *Guangzhou Medical University, Guangzhou 510095, China Corresponding author: Zhang Xibao, Email: zxibao@126.com ��Abstract�� Pityriasis rubra pilaris��PRP��is a chronic, papulosquamous inflammatory skin disease characterized by keratotic follicular papules that confluence into scattered vast erythematous squamous plaques, palmoplantar keratoderma and scurf-like scales diffusely distributed on the scalp. It often develops into erythroderma desquamativum. The pathogenesis of PRP is still unknown. At present, PRP is considered to be mainly due to a heterozygous mutation in the CARD14 gene on chromosome 17q25.3 that causes the activation of the nuclear factor-κB pathway. Moreover, the expression of p53 in epidermal cells is increased in lesions of PRP. Another hypothesis is that PRP is a T cell-mediated autoimmune hypersensitivity reaction. Additionally, keratinization abnormality, vitamin deficiency, endocrine dysfunction, liver function impairment and some infections may also contribute to the initiation of PRP. This article summarizes recent advances in the pathogenesis of PRP.