In vitro, patient-derived human induced PSC (hiPSC)–CMs with germline BRAF-activating mutations (T599R and Q257R) displayed a phenotype reflective of hypertrophic cardiomyopathy (28, 29), while in vivo mouse experiments have shown that transgenic CM–specific BRAF-V600E expression is sufficient to drive cardiac hypertrophy (16) and that BRAF is an important mediator of CM response to prohypertrophic stimuli (30). The gene discussed is BRAF; the disease is hypertrophic cardiomyopathy.