Systems model for ciliary excitation offers new avenues for mechanistic interpretation of ciliary pathologies. The systems model for intraciliary Ca2+ regulation offers new strategies for interpretation of experimental data and development of pharmaceutical interventions for ciliary motility-associated pathologies. The ciliary system is predicted to maintain either low (A) or high (B) levels of intraciliary Ca2+. The extracellular conditions can shift the functional modes of ciliary activity and cause a temporal, repetitive or a long term Ca2+ increase which causes cilia to reverse the direction of beat. The long term reversal of the direction of beat can explain the mechanism of the situs inversus disease, which is a congenital condition in which the major organs are mirrored with respect to their normal positions. Intraciliary Ca2+ levels modulate ciliary beat frequency  via either an external signal through the G-protein mediated pathways or by parametric regulation of GC activity. Such alterations can represent a physiological response to external and intracellular signals, but can also occur as a result of genetic mutations. According to our model, the latter case represents a potential pathology and in either case of permanent Ca2+-dependent CBF alteration (C or D) requires the development of therapeutic strategies to rescue the mutation-mediated alteration of the system.