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). This evidence concerns the gene BRAF and cardiac hypertrophy.