Disruption of the TRIAP1-PRELI complex reduces levels of PA transfer from the ER into the mitochondrial inner membrane and CL production, which facilitates the release of CYTC and apoptosis (Potting et al., 2013), a mechanism that possibly explains why TRIAP1 is upregulated in multiple myeloma (Park and Nakamura, 2005; Felix et al., 2009). This evidence concerns the gene TRIAP1 and AL amyloidosis.