The authors hypothesized that patients with rapid ICB clearance, increased cachexia, and poorer performance status were simply a reflection of a resistant disease cohort, rather than intrinsically causal of ICB failure.11, 40 Though biologically conceivable, this cachexia hypothesis relies on clearance calculated using a time‐dependent population PK model38 that included change in weight and albumin as some of a limited number of covariates to explain inter‐individual variability in PKs. This evidence concerns the gene ALB and Cachexia.