Notably, Pecam1 disruption (Pecam1 constitutive KO) (McCormick et al., 2015), constitutive activation of CTNNB1 (CTNNB1 deleted from its degradation domain) (Nakagawa et al., 2016), Rbpj disruption (Jabs et al., 2018) and EphB4 disruption (Luxán et al., 2019) were shown to induce systolic dysfunction characterized by increased Natriuretic Peptide A (NPPA) or Natriuretic Peptide B (NPPB), decreased EF, decreased FS and cardiac hypertrophy expect for EphB4 disruption which did induce cardiomyocyte hypertrophy but not cardiac hypertrophy. Here, RBPJ is linked to cardiac hypertrophy.