These findings revealed a potential molecular mechanism in which PIM1 mediates crosstalk between signalling pathways, including independent Smads and c-Myc, which then target downstream transcription factors (ZEB1, ZEB2, Snail1, Snail2 and Twist) to trigger EMT; moreover, hyperactivation of EMT was shown to be associated with ccRCC cell proliferation, motility and invasion, as well as angiogenesis (Fig. 7). This evidence concerns the gene SNAI1 and nonpapillary renal cell carcinoma.