Here, MID1IP1 depletion induced upregulation of ribosomal protein L5 or L11, whereas depletion of L5 or L11 activated c-Myc in MID1IP1-depleted HepG2 and Huh7 cells, implying that L5 or L11 as a tumor suppressor regulates c-Myc, which was supported by Liao et al.’s paper that ribosomal proteins L5 and L11 cooperatively inactivate c-Myc via RNA-induced silencing complex [17]. The gene discussed is MYC; the disease is neoplasm.