Furthermore, we have previously determined that the knockdown of DJ-1 inhibited human HepG2 cell growth and xenograft-induced tumor generation potentially through the Akt signaling pathway [8], and in the present study, we found that DJ-1 induced the activation of downstream Akt/mTOR, ERK1/2, and STAT3 in ECDHCC-1 cells via at least partially FGFR1, which suggested the important role of DJ-1/FGFR1 signaling pathway on the initiation, progression, proliferation, and angiogenesis in HCC vascular endothelium. Here, MTOR is linked to neoplasm.