Furthermore, two additional FAM83G pathogenic palmoplantar keratoderma mutations, which encode A34E and R52P substitutions within the conserved DUF1669 domain respectively, both led to the inhibition of CK1 binding, suggesting that the interaction between the DUF1669 domain of FAM83 proteins and CK1 appears to be more complicated than a simple binding motif [64]. This evidence concerns the gene CSNK1A1 and hereditary palmoplantar keratoderma.