We revealed a mechanism by which statin treatment can make skeletal muscles susceptible to myopathy—dissociation of the FK506 binding protein (FKBP12) from the sarcoplasmic reticulum (SR) Ca2+ release channel, the ryanodine receptor 1 (RyR1), which is accompanied by numerous spontaneous Ca2+ release events (i.e., Ca2+ sparks) (26). The gene discussed is FKBP1A; the disease is myopathy.