By contrast, in LC and CC, and in subsets of BC defined by receptor or signalling context, the prevailing RNA‐binding‐protein landscape (typified by the LIN28/hnRNP balance), together with tumour‐suppressive checkpoints and pathway tone (intact TP53/PTEN and restrained Wnt/β‐catenin) and a cap‐reader equilibrium that favours eIF4E3 over eIF4E1, biases METTL1 outputs towards miRNA‐centred repression rather than translational activation, yielding a tumour‐suppressive phenotype in LC and, under treatment conditions, chemosensitization in CC.9, 52, 66, 74. This evidence concerns the gene METTL1 and breast cancer.