Potential tumor suppressor. Acts as a KRAS-specific effector protein. May promote apoptosis and cell cycle arrest. Stabilizes STK3/MST2 by protecting it from proteasomal degradation. Interacts directly with activated KRAS in a GTP-dependent manner. Interacts (via SARAH domain) with STK3/MST2 AND STK4/MST1. Translocates to the cytoplasm in the presence of STK3/MST2 AND STK4/MST1. Widely expressed with highest levels in brain, placenta, peripheral blood and lung. Frequently down-regulated in lung tumor cell lines. Phosphorylated by STK3/MST2 and STK4/MST1. Extended N-terminus.