Positively charged residues on K8 (K8 R148/149, L159/161) are responsible for the p38 interaction; thus, K8 R148/149E, L159/161A mutation blocks the interaction, and K18 I150V, a natural mutation found in patients with liver diseases, inhibits the interaction due to its proximity to the binding site of p38 in the form of a K8/K18 heterodimer [120]. Here, KRT8 is linked to liver disorder.