Numerous studies have unraveled the common molecular alterations occurring in PC, such as mutations in Kras, p53, and BRCA1 (Nag et al., 2013; Cicenas et al., 2017; Waters and Der, 2018), aberrant activation of wnt/β-catenin signaling and keap1/Nrf2 signaling (Qin et al., 2018; Kuo et al., 2019; Qin et al., 2019), and amplification and overexpression of MDM2, cyclin D1, USP7, and MDR1 (Qie and Diehl, 2016; Robey et al., 2018; Wang et al., 2019b; Dong et al., 2020; Qi et al., 2020), which play critical roles in the initiation, progression, metastasis, and chemoresistance of PC. This evidence concerns the gene TP53 and pachyonychia congenita.