We hypothesize that partial shifting of the LL-37-mediated activity from promoting to inhibiting the growth of cancer cells resulted from increased uptake and intracellular accumulation of ROS-generating nanoparticles, which would be in agreement with previous reports indicating that human cathelicidin is able to increase the uptake and activity of antineoplastic molecules co-administered simultaneously, even in cells whose growth should be stimulated by LL-37, such as ovarian cancer cells [16]. The gene discussed is CAMP; the disease is ovarian carcinoma.