Our experiments disclosed that JPH3 acted as an oncogene in ATC cells, facilitating tumor development, and JPH3 can activate the JAK-STAT signaling pathway by upregulation of collagen type XXVI alpha 1 chain (COL26A1), and experiments attested that JPH3 promoted the proliferation, invasion, and migration of ATC cells by activating the JAK-STAT signaling pathway. This evidence concerns the gene SOAT1 and neoplasm.