PRMT5 knockdown in lung cancer (H596, H1048 and H1155), prostate cancer (Du-145) and triple-negative breast cancer (MDA-MB-436) cell lines, all harboring natural RB1 loss-of-function mutations or deletion, resulted in significant growth inhibition, accumulation of cells in G1, and a decrease in cells in S phase (Supplementary Fig. 4), further suggesting the potential applicability of therapeutic targeting PRMT5 across various types of cancer with RB deficiency. This evidence concerns the gene PRMT5 and lung carcinoma.