KIT and bacterial infectious disease: Similarly, OSI-930 treatment induced VCAM1, CCL20, and IL-8 transcription upon bacterial infection (Figure 4C, dark vs. light gray bars), suggesting that c-KIT function is required for the inhibition of key cytokines and adhesion molecules by pathogenic Yersinia. Notably, treatment of THP-1 cells with OSI-930 alone did not significantly change EGR1 transcript levels (Figure 4C, white bar), indicating that pharmacological inhibition of c-KIT did not initiate a non-specific immune response mediated by EGR1 in the absence of bacterial infection.