We also identified six UPRs unique to CPA-treated B16F10 tumors vs. GL261(B6) tumors that promote tumor cell survival or tissue repair and may contribute to B16F10 tumor unresponsiveness: activated UPRs KDM5B [32], RBL2 [33] and SPARC [34–36]; and inhibited UPRs FOXM1 [37], CD24 [38, 39] and CSF2 [40]) (Additional file 4: Table S3C). The gene discussed is FOXM1; the disease is neoplasm.