NPPB and AL amyloidosis: In AL amyloidosis, a major clue towards this conclusion came from clinical evidence; variations in the concentration of circulating amyloidogenic free LC are immediately paralleled by concordant and proportional variations of NT-proBNP concentration, a marker of cardiac damage; changes in NT-proBNP concentrations, in turn, reflect rapid improvement or worsening of heart dysfunction, even in the absence of a reduction of cardiac amyloid load, as estimated by echocardiography [14].