Notably, diminished AGR2 downregulated E-cadherin (Fig. 4k, l), and a prior study has indicated that E-cadherin downregulation may aid in the ligand-dependent activation of RTK in tumors.38,39 Together, these data unveiled that the low expression of AGR2 diminished E-cadherin expression to activate the ALK/c-MET signaling which was closely related with the enhanced response to crizotinib (Fig. 6i) in PCa. This evidence concerns the gene AGR2 and posterior cortical atrophy.