This can be explained by 1) synergistic effect from co-targeting these receptors as Lee et al. previously reported effective tumor inhibition in in vivo colon cancer models with CHIR-258, which is EGFR, FGFR, PDGFR and VEGFR inhibitor [26], 2) overlapping downstream pathways of these receptors, that might allow cancer cells to develop resistance mechanisms using alternative receptor tyrosine kinases. The gene discussed is EGFR; the disease is neoplasm.