While Salirasib blocked PRL-3 phosphatase activity in a cell-free system, it is difficult to ascribe the cellular functions of Salirasib strictly to its interactions with PRL-3—Salirasib treatment of colorectal cancer cells with PRL-3 knock-down appeared to die to an extent not seen with either PRL-3 shRNA or Salirasib treatment alone, suggesting multiple mechanisms of action for this drug, perhaps in synergy with PRL-3 loss. The gene discussed is PTP4A3; the disease is colorectal cancer.