Downregulation of endogenously expressed Bbln by transgenic expression of a Bbln-targeting miRNA under control of the ubiquitous cytomegalovirus (CMV) promoter led to decreased cardiac phospho-T287–CAMK2D contents, reduced the levels of aggregated phospho-S345–MLKL octamers as effectors of necroptosis and improved the cardiac function in heart failure induced by AAC (Fig. 8a–d). Here, BBLN is linked to heart failure.