Therefore, to ensure that the influx we measured here is ORAI-dependent, and that the residual increase is not caused by other key Ca2+ channels, we inhibited TRPC4/5 and the activity-dependent Ca2+ channel NDMAR in succession in a representative HC and BD line to assess any effects those other players may have on the disparity between HC- and BD-NPCs (Fig. S3). This evidence concerns the gene TRPC4 and Behcet disease.