The present study was conducted on human Jurkat T‐cell lines in order to elucidate the role of phospholipase A₂ in capacitative calcium entry. We have employed thapsigargin (TG) that induces increases in [Ca²⁺]_i by emptying the calcium pool of endoplasmic reticulum, followed by capacitative calcium entry. We designed a Ca²⁺ free/Ca²⁺ reintroduction (CFCR) protocol for the experiments, conducted in Ca²⁺‐free medium. By employing CFCR protocol, we observed that addition of exogenous arachidonic acid (AA) stimulated TG‐induced capacitative calcium influx. The liberation of endogenous AA and its autocrine action seems to be implicated during TG‐induced capacitative calcium influx: TG potentiates the induction of constitutively expressed mRNA of four PLA₂ isoforms (type 1B, IV, V, VI), the inhibitors of the three PLA₂ isotypes (type 1B, V, VI) inhibit TG‐induced release of [³H]AA into the extracellular medium, and finally, these PLA₂ inhibitors do curtail TG‐stimulated capacitative calcium entry in these cells. These results suggest that stimulation of three isoforms of PLA₂ by thapsigargin liberates free AA that, in turn, induces capacitative calcium influx in human T‐cells.