In this scenario, the simplest modification was based on the use of moieties known to increase protein stability, such as Fc portions or HSA.[26, 30] Alternatively, stability could be increased via chemical modifications of the protein, for example exploiting N‐glycosylation to improve the solubility and/or removing or masking cleavage sites.[34] Moreover, protein conjugation has been exploited to also improve pharmacodynamic parameters, coupling GDF15 with molecules able to give synergic anti‐obesity activity, i. e., GLP‐1.[41]. The gene discussed is GDF15; the disease is obesity due to melanocortin 4 receptor deficiency.