Although, for more than two decades, the mutation of Cu–Zn superoxide dismutase 1 (SOD1) was the only genetic aberration relevant to the initiation of familial ALS, recent studies have found more abnormalities associated with the onset of sporadic and non-SOD1 familial ALS, including a host of RNA/DNA-binding proteins such as the 43-kDa transactive response (TAR) DNA-binding protein (TDP-43) and the fused in sarcoma/translocated in liposarcoma (FUS/TLS) [5]. The gene discussed is SOD1; the disease is sarcoma.