Typical estrogen receptor (ER)-positive luminal breast cancers that overexpress either AGTR1 or PAR1 exhibit NF-κB-driven epithelial-mesenchymal transition (EMT)-associated alterations, such as increased expression of Snail, ZEB1, vimentin, and N-cadherin, downregulation of E-cadherin, as well as increased cell invasion and migration—all of which are abrogated upon silencing or pharmacological inhibition of MALT1 [84]. The gene discussed is ESR1; the disease is breast cancer.