We have also demonstrated that a lysine to arginine mutation at residue 303 (K303R) within the hinge domain of ERα may potentiate ERα’s role as an effector of leptin signaling, which results in an increased cell proliferation, migration, and invasion, thus contributing to the more aggressive phenotype of K303R-associated breast cancers [172]. The gene discussed is ESR1; the disease is breast carcinoma.