However, the proteomic investigation of CS mouse hearts revealed additional changes in proteins specifically involved in the pathophysiology of cardiomyopathy (Supplemental Figure 7), such as CRYAB, TNN or MYBPC3, suggesting that LKB1/AMPK signaling deregulation is only one mechanism contributing to the complexity of CS heart pathophysiology, as expected in a condition of HRAS/MAPK pathway overactivation. The gene discussed is CRYAB; the disease is Cowden syndrome 1.