SLC7A11 and neoplasm: Earlier studies identified adhesion molecule CD44 variant (CD44v) as a SLC7A11-binding partner that regulates SLC7A11 protein stability, and showed that CD44v inactivation leads to decreased stability and defective cell surface localization of SLC7A11, resulting in compromised SLC7A11 function in regulating GSH synthesis, redox maintenance, and tumor growth and metastasis (Ishimoto et al., 2011; Yae et al., 2012).