Junwang Xu et al. generated a mouse model with cardiomyocyte-specific deletion of neurofibromin (Nf1-cKO), finding that these mice developed significant cardiac hypertrophy, progressive cardiomyopathy, and fibrosis in adulthood, accompanied by hyperactivation of Ras and its downstream signaling pathways, indicating a critical role of NF1 in cardiac hypertrophy and dysfunction [20]. The gene discussed is NF1; the disease is cardiomyopathy.