In the current work, we employed purified WT and HCM mutant cardiac heavy meromyosin (cHMM) and S1 constructs to investigate 1) the kinetic switching and/or equilibrium state represented by single-nucleotide turnover product release and 2) how head–tail interactions, myopathy mutations, and small-molecule treatments might alter the SRX/DRX partition. The gene discussed is SRXN1; the disease is myopathy.