Fig 1H indicates that pathogenic infection caused the induction of upregulated expression of Orail and STIM1, yet only Orai1 was attenuated to some extent by 2-APB. No effect was found for other Ca2+ entry channels, such as TRPV1 expression, which is known to be activated by 2-APB stimulation [23]. It is reasonable to conclude that 2-APB interrupted the pathogen-induced increase of intracellular Ca2+ concentration via the inhibition of SOCE activity in macrophages. The gene discussed is CA2; the disease is infection.