Publisher Summary Stimuli of very diverse nature cause increases in [Ca2+]i in both T and B lymphocytes, and these increases in turn presumably give rise to a wide spectrum of cellular effects. Control mechanisms for [Ca2+]i are located both in the plasma membrane and within the cells. Changes in [Ca2+]i, in both types of lymphocytes, arise from a combination of internal store release and Ca2+ uptake across the plasma membrane. Alteration in Ca2+ efflux does not appear to play a role in the net increases in [Ca2+]i. In both T and B cells, release from internal stores is easily dissociated from Ca2+ uptake. Unlike excitable cells, Ca2+ is not transported through voltage-gated channels in lymphocytes. Instead, in both T and B cells, ligand-gated Ca2+-selective and conductive channels appear to be operative with membrane depolarization inhibiting ligand-induced entry of Ca2+. Changes in [Ca2+]i appear to be essential for some responses, contributory to some and irrelevant to others. The connection of changes in [Ca2+]I, especially due to Ca2+ uptake and receptor-activated phosphatidylinositol hydrolysis, is not entirely clear in many situations.