FAM98A encodes a protein that serves multiple regulatory functions in cellular processes and disease progression. The protein positively stimulates PRMT1-induced arginine methylation 1 and is itself a substrate for PRMT1, with five novel arginine dimethylation sites identified 2. FAM98A forms a complex with DDX1, C14orf166, and FAM98B that is required for PRMT1 expression 1. Mechanistically, FAM98A promotes cell proliferation and migration through its dimethylation sites, as dimethylation-deficient mutations suppress these processes 2. The protein also inhibits ferroptosis by activating xCT translation in stress granules 3. In cancer contexts, FAM98A is consistently overexpressed and promotes malignant progression across multiple tumor types including colorectal 13, breast 4, and endometrial cancers 56. Its expression is regulated by microRNAs including miR-26a 4, miR-142-3p 5, and miR-545-3p 6. Clinically, high FAM98A expression correlates with poor prognosis and contributes to chemotherapy resistance, particularly 5-fluorouracil resistance in colorectal cancer 3. FAM98A has also been identified as a host factor for coronavirus infections 7.