NPPB and AL amyloidosis: Amyloidogenic LCs from patients with cardiac AL amyloidosis may induce mitogen-activated protein kinase (MAPK) p38 signaling, which, in addition to mediating cardiomyocyte dysfunction and cell death, can also induce BNP transcription, supporting a possible link between the cardio toxic effects of LCs and increased natriuretic peptides release [29, 30].