LIPE and neoplasm: Therefore, in agreement with our results, it is plausible that lipid enriched TNBC cells may be as a result of altered HSL protein expression, mitochondrial dysfunction or the inhibition of mitochondrial FA oxidation induced by Doxorubicin (increased ROS), which shifts the utilization of FA away from oxidation and indirectly promotes triglyceride synthesis and subsequent lipid storage (triglyceride-rich lipid droplets) or more densely packed membranes in tumour cells [81–83].