Highlights from the article: STIM1-deficient patients have impaired T cells and NK cell function, but usually a normal distribution of the major immune cell types, including T cells, B cells, and natural killer (NK) cells with the T cell repertoire that is normally comparable with healthy individuals [[3]]. STIM1 deficiency results in no store-operated calcium entry (SOCE) in T cells and as a result the patient's cells cannot respond appropriately to T cell receptor (TCR) activation or pharmacological agents, such as ionomycin and thapsigargin (TG), which typically trigger Ca SP 2+ sp influx [[1]]. We used Western blot to investigate the expression of STIM1 in the patient's (P1) PBMCs and failed to detect either the full length or the truncated variant of STIM1. It is interesting that lack of calcium flux seen in the patients' T cells, either due to total lack of full length STIM 1 expression or due to truncated STIM1, has not resulted in a more profound immunodeficiency.