A new study found that inhibition of NOP56, a ribosomal protein that plays a role in ribosomal assembly, leads to impairment in the response to ROS, therefore KRAS-mutant cells shifted their metabolism toward the mTOR pathway, and co-inhibition of NOP56 and mTOR led to tumor regression in xenograft mouse models [87,88]. Here, KRAS is linked to neoplasm.