FKBP1B and catecholaminergic polymorphic ventricular tachycardia: This hypothesis is attractive because CPVT episodes occur by definition during adrenergic stimulation, and normal phosphorylation of RyR2 channels by PKA (the main kinase linking β-adrenergic stimulation to cellular effects) is presumed to dissociate FKBP12.6 from RyR2 [29].