For instance, a study on MKP-1 showed that MKP-1 knockout mice had lower ERK activation and manifested better protection against the development of obesity when fed with a chow diet as compared to wild type, and displayed reduced adiposity.[91] However, inhibition of MKP-1 using antisense oligonucleotides resulted in the sustained activation of ERK1, which led to reduced adiposity, contrary to findings reported in MKP-1 knockout mice. The gene discussed is MAPK1; the disease is obesity due to melanocortin 4 receptor deficiency.