Tumor-specific knockdown of CCR9 resulted in increased activation of STAT signaling in T cells, in changes of gene expression that correlated with better and improved T cell effector functions, and in increased production of Th1 cytokines (IFN-γ, IL-2, and TNF-α) by antigen-specific CTLs, all of which have been shown to correlate with prolonged CTL survival and in vivo tumor rejection (Fallarino & Gajewski, 1999; Yu et al, 2009; Wilde et al, 2012). The gene discussed is SOAT1; the disease is neoplasm.