Through the years, different models have been proposed in order to explain both FAM46C tumour suppressor phenotypes and its physiological role: the poly(A) polymerase model [20], in which FAM46C is proposed to polyadenylate the poly(A) tails of specific transcripts, stabilizing them; the PLK4 regulator model [9], in which, by inhibiting PLK4 activity, FAM46C is envisaged to restrict centriole over-duplication; and the intracellular trafficking model [21], in which FAM46C is proposed to function as a master regulator of intracellular trafficking dynamics. This evidence concerns the gene TENT5C and neoplasm.