Cholesterol efflux pathways have anti-inflammatory and anti-proliferative properties that could be exploited in tumor biology to unravel cancer vulnerabilities. Using a mouse model of lung tumor bearing KRASG12D mutation, the inventors identified that disruption of cholesterol efflux pathways by specific inactivation of Abca1 and Abcg1 in epithelial cancer progenitor cells and to some extent in macrophages promoted a pro-tolerogenic tumor microenvironment (TME). In particular, the inventors show that cholesterol removal therapy with cyclodextrin inhalation also reduced tumor burden in progressing tumor by suppressing the proliferation and expansion of epithelial progenitor cells of tumor-origin. The inventors’ results position cholesterol removal therapy as a putative metabolic target in lung cancer progenitor cells. The present
invention relates to a method for the treatment of a lung cancer in a patient in need thereof comprising administering to the patient a therapeutically effective amount of cyclodextrin.