In addition to activation of the UPR machinery, high Bcl-xL expression may promote survival of invasive tumor cells during the metastatic process; for example Bcl-xL has been reported to be a suppressor of anoikis, [15, 21] which would explain its association with increased risk-of-relapse in the BRAFMT subgroup. Here, BCL2L1 is linked to neoplasm.