NFAT1 deficiency in chondrocytes leads to an increased prosurvival and proinflammatory phenotype. (A) Immunoblot of EV- and WT NFATC2–transduced patient chondrocytes before and after 15 minutes of P/I stimulation, 20 ng/mL IL-1β stimulation, or no treatment (n = 3). (B-D) RNA sequencing carried out on EV- or WT NFATC2–transduced patient chondrocytes unstimulated or stimulated for 24 hours with P/I or 20 ng/mL IL-1β. (B) Venn diagram of significantly (FDR < 0.05) upregulated (Bi) and downregulated (Bii) genes in EV-transduced patient chondrocytes compared with WT NFATC2–transduced chondrocytes. (C) Heat map of top genes that meet a FDR < 0.025 cutoff between EV and WT NFATC2–transduced patient chondrocytes. (D) Heat map of sample level enrichment scores with normalized enrichment scores, P-value, and q-values for each pathway determined by gene set enrichment analysis. Min and max refer to the row-normalized minimum and maximum for each pathway. (E) Measurement of percent cell death in chondrocytes over 12 days by quantifying LDH in supernatants. ∗P < .05, ∗∗∗P < .001, two-way analysis of variance, Dunnett’s post-hoc test. (F) Enzyme-linked immunosorbent assay detection of IL-6 production from the supernatants of chondrocytes in different conditions. ∗P < .05, ∗∗∗P < .001, Mann-Whitney U test. NS, not significant.