They corresponded to cell fate determination, cell cycle activation, epigenetic modifications, DNA damage response, as well as cancer-related pathways including Wnt/β-catenin, PI3K/AKT/mTOR, Slit2/Robo1, MYC, and ErbB2-ErbB3 axes (Figure 1C and Supplementary Table 1). This evidence concerns the gene SLIT2 and cancer.