Store-operated calcium entry (SOCE) plays an important role in platelet function. It is generally assumed that the mechanism of SOCE relies on the direct interaction of STIM1 and ORAI1 proteins with specific STIM1:ORAI1 stoichiometry. However, in platelets, other pathways may take place. Here we aim to investigate the mechanisms of SOCE in platelets. We developed a lattice-based mathematical model that represented STIM1-ORAI1 interactions and applied it to both HEK cells, where SOCE mechanism is well established, and platelets. The model was able to describe STIM1-ORAI1 behavior in HEK cells successfully. We used the same parameters for protein interaction and applied them to platelets. As a result, we demonstrated that the number of STIM1 proteins on ER membrane could not assure the needed stoichiometry to proper SOCE in platelets.