Mechanistically, the tumor-suppressive effect of ANLN knockdown on prostatic carcinoma cell growth is partially reversed by IGF2BP1 overexpression, indicating that ANLN facilitates prostate cancer progression by stabilizing the proto-oncogene c-Myc through IGF2BP1 and activating the MAPK signaling pathway (Liu et al., 2024). The gene discussed is IGF2BP1; the disease is prostate carcinoma.