IGF2BP2 and cancer: We then directly examined the biological cross-talk between LCAT1 and IGF2BP2, and found that growth suppression, triggered by LCAT1 knockdown, as we previously shown [19], could be largely reversed by IGF2BP2 overexpression (Fig. 3J), suggesting that the biological effect of LCAT1 on cancer cell growth is mediated, at least in part, through IGF2BP2.