Collectively, all these data suggest that BSDL variants (BSDL-InsC, CEL-MUT, CEL-HYB, BSDL-J28+, and any other not yet characterized variant that cannot be detected by mass sequencing or “omics” studies) that are expressed and retained within acinar cells, or present in blood circulation and captured by any cell within the tumor, could be implicated in the cellular lipid metabolism reprogramming observed in pancreatic pathologies [204, 206–208]. Here, CEL is linked to neoplasm.