IFN-α treatment-responsive clones display high ribosomal activity. (A) Mitochondrial variants were used to analyze clonality from the scRNA-seq data. For each included sample, the profile of mitochondrial variants of interest and their combination to identify clones is shown. (B) The number of identified clones (effective number of species) was compared between PV and HC samples. Differences were analyzed using the Kruskal-Wallis rank sum test. (C) Identified clones in the untreated and treated condition of PV samples were compared. In 2 patients with PV, clones were identified in which the cell number was strongly decreased, termed vanishing clones, and the DEGs of these were analyzed. The Venn diagram depicts the number of DEGs in both patients. (D) Gene ontology (GO) terms were derived from the DEGs that were identified in both PV samples. The 5 most up- or downregulated pathways are shown. (E) Differential regulation of the genes derived from the DEGs was compared between the HC and PV samples. For each gene and group, the FC was calculated and directly compared between the HC and PV samples. Statistical analysis was done using a Wilcoxon rank sum test. ∗∗∗∗P < .0001. (F) Single clones (from supplemental Figure 4) were stimulated with IFN-α, and the FC was calculated following IFN-α treatment. Differences were analyzed using Wilcoxon rank sum tests. (G) The PBMC fraction from patients with PV were harvested and used for RNA isolation. Patients were grouped according to therapy into IFN-α only, which included IFN-treated patients, and all others were grouped together as various therapies. The STAT1 and RPL18A expression was analyzed using RT-qPCR. Statistical analysis was done using Mann-Whitney tests. ∗∗P < .01.