This selectivity may be partially explained by the differential stress signaling and survival pathway addiction in malignant cells, whereby HF preferentially engages pro-apoptotic networks such as ROS–JNK–p38, mitochondrial apoptosis, and NF-κB suppression in highly proliferative, oncogene-driven tumor cells, whereas quiescent or mildly stressed normal cells exhibit higher tolerance and require higher HF concentrations to undergo cytotoxic responses. Here, NFKB1 is linked to hydrops fetalis.