SMAD4 and pachyonychia congenita: Genetic alternations, for example, in KRAS, TP53, CDKN2A, and SMAD4,2 (as the main drivers of PC), appearance of numerous differentially up- and downregulated genes, and downstream affected cellular signaling pathways have long been shown to be involved in PC progression (Jones et al., 2008; Javadrashid et al., 2021).