On the basis of the hypothesis here presented, the therapy of cardiovascular risk factors (hypertension, hyperlipidemia, insulin resistance/T2D) should pay attention first to a decrease in the pathogenetically underlying increased tissue stiffness (e.g., activity reduction of ENaC, RhoA, F-actin, and YAP/TAZ) instead of a meticulous correction of surrogate quantities hypertension, hyperglycemia, and hyperlipidemia. The gene discussed is RHOA; the disease is type 2 diabetes mellitus.