We argue that the gating of the ryanodine receptor (RyR) channels, key molecular determinants in the Ca2+ homeostasis, recognized as important novel therapeutic targets, is determined by electron-conformational transformations described by a simple electron-conformational model (ECM).The model differs from conventional markovian models in several points, in particular, these are the RyR energy, inter-RyR coupling, conformational dynamics and unconventional quantum effects.The model describes the RyR gating under varying cis and trans [Ca2+] with the same set of the parameters.We present an overview of computer modeling of the stochastic RyR2 gating in cardiomyocytes and sinoatrial node cells (SANC). The model does explain main features of the in vitro single RyR dynamics including modal gating and adaptation phenomena, effect of the cis[Ca2+] and cis[Mg2+], the temperature effects. Cooperative dynamics of the RyR clusters in Ca release units (CRU) and the Ca2+ spark features have been studied in a series of model simulations for 11x11 square RyR lattice incorporated into the cell calcium dynamics. The model does explain and describe the spontaneous oscillatory regime of the CRU both in SANCs (so-called Ca2+ clock) and in cardiomyocytes under Ca2+ sarcoplasmic reticulum overload. Puzzlingly, the intracellular clock obeys the Bowditch behavior without any membrane clock assistance. Given strong enough RyR-RyR coupling we observed novel effect of sudden inhibition of the oscillations with emergence of stable subclusters (2x2, 2x4,…) of opened channels and a steady-state Ca2+ leakage. The CRU oscillatory regime is restored by external membrane stimuli, so only working synergistically two types of clocks ensure robust and flexible pacemaker function. Despite the ECM is intentionally simplistic, it offers novel insight into the actual physical mechanisms involved in the gating behavior of the RyR channels with a sound framework for future studies.