Twelve‐month old male mice of p16INK4a (hereafter p16) knockout (p16−−) and wild‐type (WT), ApoE knockout (ApoE−−) and ApoE−−p16−− were fed a HFD to induce obesity, and the effects of treatment with the senolytic drug ABT263 or the SGK1 specific inhibitor EMD638683 on fibrosis, inflammaging, gene expression, integrin‐inflammasome signalling and metabolism were examined. This evidence concerns the gene SGK1 and obesity due to melanocortin 4 receptor deficiency.