A decade ago the panjunctional sarcoplasmic reticulum hypothesis was proposed (van Breemen et al., 2013), that incorporated the idea that a network of tubules and quilts capable of auto-regulating their calcium content and determining junctional calcium concentration through loading and unloading at membrane‑membrane nanojunctions. By this mechanism it was postulated that local calcium signals could be targeted to control a variety of cellular processes, from contraction and metabolism to transcriptional activities. In accordance with this, we recently identified a cell-wide network of distinct cytoplasmic nanocourses with the nucleus at its centre, demarcated by nanojunctions (<400 nm across) between sarcoplasmic reticulum (SR) and other organelles, that restrict calcium diffusion and thus provide for signal segregation in a manner facilitated by nanocourse-specific calcium pumps and release channels (Duan et al., 2019). Ryanodine receptor subtype 1 (RyR1) supports relaxation of arterial myocytes by unloading calcium into peripheral nanocourses delimited by plasmalemma-SR junctions, fed by sarco/endoplasmic reticulum calcium ATPase 2b (SERCA2b). Conversely, stimulus‑specified increases in calcium flux through RyR2/3 clusters selects for rapid propagation of calcium signals throughout deeper extraperinuclear nanocourses and thus myocyte contraction. Beyond these, nuclearenvelope invaginations and SERCA1 demarcate further diverse networks of cytoplasmic nanocourses that receive calcium signals through discrete RyR1 clusters that do not freely enter the nucleoplasm, yet impact gene expression through epigenetic marks segregated by their associated invaginations. Critically, this circuit is not hardwired and remodels for different outputs during cell proliferation.  Regardless of their functional subdivision, within cytoplasmic nanocourses all path lengths from calcium release site to targeted signalling complex are on the nanoscale. With picolitre volumes of cytoplasm lying within the boundaries of each nanocourse, relatively small net increases in local calcium flux (1-2 ions per picolitre) will be sufficient to raise the local concentration into the affinity ranges of most cytoplasmic calcium binding proteins (Fameli et al., 2007; Fameli et al., 2014). It is intriguing, therefore, that recent studies have established that unicellular organisms employ sequential computational logic to engage behaviour selection (Dexter et al., 2019). Sequential logic can be actioned by progression through a series of circuit memory elements called flip‑flops, which store a single bit (binary digit) of data, by switch and reset between 0 and 1. By analogy I propose that nanocourse-specific calcium binding proteins operate as local “switches”, their position and reset directed, in part, by changes in local calcium flux. In this way coincident increases in calcium flux could be triggered in two distant parts of the cell-wide web at the same time (Duan et al., 2019), enabling coordination of multiple cellular functions through either sequential, or parallel logic processing. This draws obvious parallels to mechanisms of conduction in carbon nanotubes, that transmit charge carriers through discrete conduction channels, enablingmemory, logic and parallel processing. Thus, by analogy, our observations point to the incredible signalling potential that may be afforded by modulating “quantum calcium flux” on the nanoscale, in support of network activities within cells with the capacity to permit stimulus-dependent orchestration of the full panoply of diverse cellular processes.