Specifically, PPDs/PPDQs disrupt the MAPK–cancer–calcium signaling axis, where calcium influx via TRPM8 synergizes with EGFR/SRC to amplify proliferative signals, while calcium overload concurrently activates CASP3-dependent apoptosis: a bistable imbalance driving inflammation and carcinogenesis, as evidenced in zebrafish models. Here, CASP3 is linked to cancer.