This indicates a novel mechanism for the anti-tumor activity of fucoidan, namely inhibiting tumor viability by activating the TLR4/ROS/ER stress axis and the downstream PERK-ATF4-CHOP pathway (i.e., via the TLR4/ROS/PERK/eIF2α axes) [48], leading to apoptosis and suppression of lung cancer cell progression in vitro and in vivo. Here, ATF4 is linked to neoplasm.