Most notably, Fhl1-/- mice subjected to transverse aortic constriction (TAC) maintained cardiac function comparable to sham-operated control mice, and unlike control mice, which exhibited pathological cardiac hypertrophy and dysfunction (Sheikh et al., 2008), highlighting that loss of FHL1 is essential for preservation of cardiac function in pressure overload. The gene discussed is FHL1; the disease is cardiac hypertrophy.