The overexpression of SH3BGR, which mimics DS condition, significantly activates cardiomyocyte hypertrophy via RhoA/SRF signaling, whereas SH3BGR knockdown abrogates cellular hypertrophy, leading to a combination of sarcomeric dysfunction, activation of apoptosis and reduced cell viability via alterations in the RhoA/SRF and Hippo signaling pathways in cardiomyocytes (Figure 5). The gene discussed is SRF; the disease is Dravet syndrome.