SOAT1 and neoplasm: Potential molecular mechanisms include: Modulating tumor-derived immunoregulatory factors via m6A modification to influence the recruitment and activation of T cells, macrophages, and dendritic cells; Regulating key transcription factors or signaling pathways within immune cells-such as NF-κB, JAK/STAT, or HIF-related pathways-to alter the magnitude and type of immune responses; Collaborating with other m6A enzymes to form regulatory networks that impact tumor–immune cell interactions.