Taken together these data indicate that the reduced activation of DDR observed when RanBP9 is silenced results in an enhanced sensitivity of lung cancer cells to different genotoxic stress in a cellular context-dependent manner, and that different pathways, including, at least in part, ERK1/2 and AKT, might be involved in the RanBP9-dependent regulation of cellular DDR, proliferation and apoptosis. The gene discussed is AKT1; the disease is lung carcinoma.