It also promoted apoptosis, inhibited constitutively active STAT3, modulated STAT3 activation by modifying the activity of upstream STAT3 regulators, and abrogated IL-6-induced STAT3 activation, thereby suppressing the JAK/STAT pathway in various cancer cells, such as tongue squamous cell carcinoma (HN-9), hypertriploid renal cell carcinoma (786-O), and oral squamous cell carcinoma (YD-8) [154]. Here, SOAT1 is linked to cancer.