CXCR1 and neoplasm: At 3 dpf, no additive effect was observed in Rac2D57N mutants treated with SB225002 compared to DMSO controls (Figure S2), suggesting that the proliferation reduction observed in SB225002 is primarily due to the lack of neutrophils in the microenvironment and not due to other cell types within the microenvironment or astrocyte-intrinsic effects. These data demonstrate that Cxcr1/2 promotes proliferation of tumor-initiating astrocytes and suggests that this proliferation is due to Cxcr1/2-mediated neutrophil recruitment.