Calcium signaling plays a major role in sepsis progression and has been considered as a therapeutic target since clinical evidence supports the use of blockers of several types of calcium channel, such as slow N-type, L-type and T-type voltage-dependent calcium channels, dihydropyridine calcium channel, and stromal interaction molecule 1 (STIM1)-mediated store-operated Ca2+ entry (SOCE), among others, for improving the outcome of septic patients [93–97]. The gene discussed is STIM1; the disease is Sepsis.