Unlike the phenotype of the Clk1 knockout mice reported here, overexpression of CLK2 in the mediobasal thalamus can partially reverse the HFD-induced obese phenotype in mice (Quaresma et al., 2017), and mice lacking Clk2 in adipose tissue exhibited exacerbated obesity (Hatting et al., 2017). Here, CLK2 is linked to obesity disorder.