In contrast, other studies reported that cardiac-specific NOX4 overexpression preserved cardiac function and reduced hypertrophy after 9 weeks of TAC, whereas systemic or cardiac-specific NOX4 deletion in that context worsened cardiac remodeling [28,29] (Table 1 and Table 2), pointing instead to a protective role for NOX4. The gene discussed is NOX4; the disease is cardiac hypertrophy.