The majority of ALS cases which have been reported are sporadic (SALS); 10% are familial (FALS), some of which arise from mutations in superoxide dismutase-1 (SOD1) [4], TAR DNA-binding protein (TDP43) [5, 6] and fused in sarcoma/translated in liposarcoma (FUS/TLS) [7, 8], ALS2 [9, 10], dynactin [11], and senataxin [12]. Here, TARDBP is linked to liposarcoma.