Two new obese mouse models for BBS include a gene trap allele (Bbs5−/−) thought to be a congenital null mutation and a conditional (Bbs5flox/flox) allele of Bbs5. Interestingly, the Bbs5 conditional mutants become obese, independent of the age of Bbs5 loss implying homeostatic roles for Bbs5 in energy homeostasis (Bentley-Ford et al., 2021; Bentley-Ford et al., 2022). This evidence concerns the gene BBS5 and Bardet-Biedl syndrome.