However, the following evidence indicates that paraptosis may not be a major contributor to CDDO-Me–induced cell death in breast cancer cells: 1) CDDO-Me–induced vacuoles were mainly derived from the ER, whereas mitochondria may be fragmented after transient fusion; 2) CDDO-Me–induced vacuolation and subsequent cell death were not inhibitable by the protein synthesis inhibitor cycloheximide; and 3) Alix was not downregulated by CDDO-Me. This evidence concerns the gene PDCD6IP and breast carcinoma.