Figure 3C confirmed the results obtained after ATG1 knock-down that glioma cells display a basal lipophagy and PARPi induced an accumulation of LDs in autophagosome, but did not increase after inhibition of autophagy, suggesting that LDs induced by PARPi are degraded but not necessarily through lipophagy. Overall, these results suggest that PARP inhibition is contributing not only to LDs formation (Figure 3A and Figure S4) but also to their turnover and utilization (Figure 3B,C). Here, ULK1 is linked to glioma.