The summary of the high cumulative 131I dose-induced cardiotoxicity mechanism in DTC/−T2DM patients would be as follows: (i) high-cumulative 131I doses trigger acute inflammation; (ii) inflammation leads to vascular permeability changes, which can cause fluid accumulation, myocardial degeneration, and capillary cell damage; (iii) the ST2-IL33 pathway is activated, leading to cardiac fibrosis, myocardial hypertrophy and stiffening and impaired heart function; (iv) increased wall stress and ventricular stretch, reflecting ventricular overload; and (v) cardiomyocyte necrosis and damage. The gene discussed is IL1RL1; the disease is cardiac hypertrophy.