Acquired mutations (A573V, V722I, A572V, A573V, H583Y, and G589D) in the JAK3 pseudokinase domain resulted in constitutive JAK3 activation. STAT3 missense single-nucleotide variants (S614R, G618R, and A702T) and STAT5B missense mutation were located in the SH2 domain, which was critical for STAT activation and further promoted growth, survival and invasiveness of tumor cells. Constitutive JAK3 phosphorylation on tyrosine 980 was also involved in JAK3 activation. This evidence concerns the gene SOAT1 and neoplasm.