We found that the phosphorylation of c-jun (P = 0.002) and STAT1 (P = 0.032) was significantly inhibited in CALCR-depleted cells compared to the respective control cells (Figure 6B), reminding that c-jun and STAT1 related signaling pathways may be involved in CALCR induced renal carcinoma development. Here, STAT1 is linked to renal carcinoma.