Given that the CARM1 methylation site on NFIB is critical for SCLC cell growth in xenograft mouse models and that knockdown of CARM1, treatment with CARM1i, or loss of the NFIB methylation site leads to better survival in these models, targeting CARM1 provides a therapeutic avenue to reduce NFIB oncogenic activity in SCLC (49). This evidence concerns the gene NFIB and small cell lung carcinoma.