Excessive ROS generation not only reflects oxidative burden but can actively drive oncogenic signaling by modulating pathways such as PI3K/Akt, JAK/STAT, MAPK, NF-κB, and Nrf2, creating a hostile biochemical environment that promotes inflammation, sustains proliferation, invasion, angiogenesis and tumor progression [29,30,31]. Here, SOAT1 is linked to neoplasm.