Although it has been previously shown that Smarca4 (Brg1) was essential for early embryonic development in mice and could compensate for the nonessential Smarca2 (Brm) (LeGouy et al., 1998), but not the other way around, a study by Strobeck et al. (2002), showed that SMARCA2 (BRM) could in fact compensate for loss of SMARCA4 (BRG-1) in a retinoblastoma cell line. Here, SMARCA2 is linked to retinoblastoma.