BCL-xL is a mitochondrial protein that acts to suppress the programmed cell death response of apoptosis, and is overexpressed in some cancers, as well as in senescent cells. Thus small molecules that bind to BCL-xL have been used as chemotherapeutics and more recently as senolytics that selectively destroy senescent cells.
That removal of senescent cells is a legitimate rejuvenation therapy that quite literally turns back aging in animal models has caused greater attention to be given to BCL-2 family proteins and their role in allowing cells to hold back apoptosis.
Separately, as noted here, evidence shows that BCL-xL is a longevity-associated protein, which is interesting, to say the least. This may or may not have anything to do with suppression of apoptosis – or if it does, one has to argue that keeping apoptosis-inclined cells alive for longer is on balance beneficial, despite being detrimental in the matter of senescent cells, or that apoptosis is complex and situational.
This may be the case, but it is always challenging to tease out the specific contributions to any observed outcome of this nature. Another possibility is that greater levels of BCL-xL improve mitochondrial function in some way, but more work is needed to establish whether or not this is a plausible mechanism.