Taken together, our attempt to induce an efficient global deletion of LAT4 past the postnatal phase was not successful because the induced LAT4 deletion was not uniformly efficient in target organs, preventing us from understanding whether the generalized lack of this AA transporter would lead to a severe malnutrition‐like phenotype also in later life, as it did in newborn mice (Guetg et al. Here, SLC43A2 is linked to nutritional deficiency disease.