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). Here, PIM1 is linked to nonpapillary renal cell carcinoma.