Cardiomyopathic troponin mutations predominantly occur at its interface with actin and tropomyosin.

It contains almost all of the sites where pathogenic substitutions occur in TnI, a highly significant result (P < 0.0001).

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One can detect borderline significance, but only by resorting to consideration within TnT only; the 15.6% pathogenic residue density in this helix is higher than the 8.7% density in TnT overall (P = 0.03).

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From the current dataset, the anchoring helix has a greater pathogenic substitution site density than does TnI-TnT overall (10.2%), but this did not reach statistical significance (P = 0.10).

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