To address if this is the case for L583R, we inhibited the proteasome activity with MG132 and observed that, despite the different initial levels of E-cadherin, the expression of mutant L583R is completely restored upon treatment (Figure 4C), indicating that it is prematurely degraded by the proteasome after synthesis, as previously described for other juxtamembranar HDGC-associated E-cadherin mutations [35]. This evidence concerns the gene CDH1 and Familial gastric cancer.