Interestingly, a recent report of a mouse model for the myosin rod disease Laing distal myopathy showed that substitution of a proline in the tail shifts myosin heads from a super-relaxed state to a disordered relaxed state, which is more capable of ATP hydrolysis and hypercontractility (Buvoli et al. 2024). The gene discussed is MYH14; the disease is glycogen storage disease VI.