BCL2L1 and cardiomyopathy: In a recent rodent study, Keller et al. disrupted the 5’ alternative splicing site in the Bcl2l1 gene to inhibit alternative splicing of Bcl-x short-isoform (Bcl-xS) in mice in vivo, and demonstrated that the suppression of Bcl-xS induces systemic inflammation, splenomegaly, cardiac fibrosis, and cardiomyopathy.