Lee et al. (2022) discovered that PLD could be a potent anti-glioblastoma multiforme (GMB) drug. However, an opposing viewpoint was proposed that PLD was an autophagy inhibitor. Researchers found that the LC3B-II level was increased while the p62 level was increased simultaneously. The autophagy regulation was related to a high abundance of LDLR in GBM cells instead of via the PI3K/AKT/mTOR or MAPK signaling pathway. It was PLD that promoted the uptake and accumulation of cholesterol in lysosomes so that the death of GBM cells was led (Lee et al., 2021). The gene discussed is AKT1; the disease is glioblastoma.