While the precise manner in which ARHGDIA regulates apoptosis/cell survival in human cancer is not known, studies in cultured rodent insulinoma cells show that overexpression of ARHGDIA increased cell viability and decreased activated c-Jun N-terminal kinase (JNK) expression following exposure to the apoptosis promoter mycophenolic acid (MPA), whereas knockdown of ARHGDIA (via RNAi) enhanced MPA-induced cell death and increased the activation of JNK[39]. This evidence concerns the gene MAPK8 and cancer.