(A) Gene expression of MHC class I (MHC I) and type I interferon (IFN) signaling genes from RNAseq of KitV558Δ/+ mice treated for 3 weeks with imatinib or vehicle. Each column represents an individual mouse. (B) Antigen processing and presentation and JAK/STAT signaling pathway gene set enrichment following RNAseq of KitV558Δ/+ mice treated with 3 weeks of imatinib; enrichment score (ES), normalized enrichment score (NES), false discovery rate (FDR) and family-wise error rate (FWER) are shown. (C) Tumor cells (CD45–Kit+) and (D) immune cells (CD45+) from KitV558Δ/+ mice treated for 1 or 4 weeks of imatinib (IM) analyzed for MHC class I expression by mean fluorescence intensity (MFI) represented on logarithmic scale. Unpaired two-sample t-test of imatinib treatment performed against untreated KitV558Δ/+ controls. Data represent mean ± SEM, * p-value < 0.05, ** p-value <0.01, *** p-value <0.001. N= 5 mice/group, repeated twice. (E) RT-PCR of Ifnb1 from bulk KitV558Δ/+ tumors after 1 and 3 weeks of imatinib treatment. Gene expression calculated relative to untreated KitV558Δ/+ tumors. (F) RT-PCR of Ifnb1 expression of sorted cells from KitV558Δ/+ tumors treated with 2 weeks of imatinib or vehicle. Tumors were separated into tumor cells (Kit+), stromal cells (CD45–Kit–), macrophages (F480+) and other immune cells (F480–). Gene expression calculated relative to Kit+ cells from untreated mice. Unpaired non-parametric Mann Whitney U test performed against control Kit+ cells. N=3 mice/group. (G) RT-PCR of Ifnb1 expression of bulk tumor from KitV558Δ/+ mice treated with two weeks of anti-CSF1R (400 μg/mouse) or isotype with gene expression calculated relative to isotype control. N=6 mice/group. (H) Tumor cells from imatinib-resistant KitV558Δ/T669I/+ mice treated with 2 weeks of imatinib and analyzed by flow cytometry for MHC class I expression, n=3 mice/group. Bulk tumor from same experiment was used for RT-PCR of Ifnb1 and gene expression calculated relative to untreated KitV558Δ/T669I/+ mice.