Our lab and others described that mutant KRAS activation/extinction in preclinical lung cancer (LC) models directly controls the expression of genes involved in β-oxidation and de novo lipogenesis, and that this can be exploited for therapeutic gain (Padanad et al., 2016; Gouw et al., 2017; Bartolacci et al., 2021). Here, KRAS is linked to laryngotracheoesophageal cleft.