The kinase inhibition profile of 3 (Table 3) resembles that of the parent compound 2–3 (Table 2) with at least two notable exceptions: 3 inhibits CSF1R, PDGFRB, and FLT3, receptor tyrosine kinases and orthologs of Drosophila Pvr that activate the Ras/ERK signaling pathway [25] and play key roles in SRC activation and tumor progression; 3 inhibits Aurora kinases AURKB and AURKC (Drosophila ortholog aurA or aurB). The gene discussed is SRC; the disease is neoplasm.