The development of SPEM and the growth of gastric tumors are inhibited by genetically removing Cd44 or using sulfasalazine, which is an inhibitor of xCT‐dependent cysteine transport.[50, 51] Chief cells must control mitochondrial activity in response to ROS using a PGC1α‐xCT‐GPX4 axis and failed ROS scavenging blocks SPEM and promotes cell death by ferroptosis.[52] An additional research group discovered that the MEK inhibitor Selumetinib is also efficacious in the treatment of SPEM. This evidence concerns the gene PPARGC1A and gastric neoplasm.