The mouse homolog of SUSD2 (susd2/mSVS-1) was first studied in 2007 by Sugahara and colleagues, demonstrating that overexpression of susd2 in HT1080 fibrosarcoma cells and HeLa cervical carcinoma cells correlated with decreased clonogenicity, anchorage-independent growth, migration, and invasion through matrigel, implicating susd2 as a potential tumor suppressor [9]. The gene discussed is SUSD2; the disease is cervical carcinoma.