However, since TRPM7 channel activity was impaired in the TRPM7+/Δkinase mice [220], it is plausible that the disrupted TRPM7 channel function during the developmental stage (E9.5 to E12.5) may have contributed to the impaired heart function, resulting in the observed cardiac hypertrophy, inflammation, and fibrosis in the TRPM7+/Δkinase mice [219]. The gene discussed is TRPM7; the disease is cardiac hypertrophy.