AKT1 and acute myeloid leukemia: CLDN4 is a target of the Claudins protein family, and nuclear translocation of CLDN4 enhances the epithelial-mesenchymal transition phenotype, resulting in the replacement of CLDN4 tightly linked with Yes-associated protein (YAP) and zonular atresin (ZO-1), forming a nuclear translocation complex, which is one of the mechanisms of renal cancer formation.[35] Research by Hu et al[36] demonstrates that CLDN4 suppression in Acute Myeloid Leukemia leads to decreased activity of AKT and ERK1/2.