Recently, chronic (i.e., 10 weeks) intraperitoneal administration of the novel PORCN inhibitor, CGX1321, was shown to attenuate both cardiac hypertrophy and fibrosis and improve cardiac function in an experimental “two hit” (both metabolic and mechanical stress) model of HFpEF via the mitigation of both canonical and non‐canonical Wnt signaling [22], demonstrating that the targeting of these signaling pathways represents a viable therapeutic target for HFpEF. The gene discussed is PORCN; the disease is cardiac hypertrophy.