Importantly, the RS constructed in our study is based on the expression profiles of four key genes—ARHGEF35, GSN, ELANE, and AKT3—which collectively provide a robust framework for elucidating the mechanistic underpinnings of RCD dysregulation in AML and pave the way for subsequent in-depth analyses of their individual contributions. The gene discussed is GSN; the disease is acute myeloid leukemia.