Understanding the mechanisms of calcium (Ca 2þ ) deficiency disorder development in plants has been a challenge for more than a 100 years. Previous studies support the hypothesis that Ca 2þ deficiency disorders can be triggered by mechanisms that reduce plant Ca 2þ uptake from the soil, fruit Ca 2þ uptake from the plant, and Ca 2þ translocation within the fruit, and also result in abnormal regulation of cellular Ca 2þ partitioning. Plant Ca 2þ uptake can be determined by Ca 2þ content and availability in the soil, root growth, activity of apoplastic and symplastic pathways of root Ca 2þ uptake, as well as uptake competition between Ca 2þ and other nutrients. Fruit Ca 2þ uptake is determined by Ca 2þ content in the xylem sap, and xylem/phloem ratio of fruit sap uptake, which is affected by the rates of leaf and fruit transpiration and growth. Calcium translocation to distal fruit tissue, containing the lowest fruit Ca 2þ content and the highest susceptibility to Ca 2þ deficiency disorders, is potentially dependent on the cell wall Ca 2þ -binding capacity and symplastic Ca 2þ uptake by the tissue at the peduncle end of the fruit, abundance of functional xylem vessels connecting peduncle and distal fruit tissues, as well as the hydrostatic gradient required for Ca 2þ translocation towards the distal tissue. Cellular Ca 2þ partitioning is defined by the activity of Ca 2þ channels, Ca 2þ ATPases, and Ca 2þ exchangers present in cellular membranes, as well as the capacity of the cell wall to bind Ca 2þ , and the formation of Ca 2þ precipitates in different cellular compartments. Therefore,