Although the deletion of COOH-terminal residues from rat CRYBB2 [35], chicken CRYBB1 [36], and human CRYBB1 [37] did not significantly impair solubility or the ability to form dimers in vitro, all known mutations (such as G220X CRYBB1 [18], Q223X CRYBB1 (in this study), Q155X CRYBB2 [22,23] and del185QSVR188 CRYBB2 [38]) suggest that disruption of the fourth Greek key motif in CRYBB1 or in CRYBB2 results in β-crystallin instability and/or cataract disease. The gene discussed is CRYBB2; the disease is cataract.