Likewise, experimental work with G93 mice (with a SOD1 mutation linked to familial ALS) and samples from ALS patients revealed that the abundance of uPAR increased in the ventral horn of the spinal cord of ALS patients and G93 mice, along with enhanced uPA-dependent plasminogen activation in advanced stages of this disease. The gene discussed is SOD1; the disease is amyotrophic lateral sclerosis.