Mechanistically, tumor‐released particles induced an increase in the levels of cAMP, followed by the activation of protein kinase A (PKA) (as indicated by the phosphorylation of its substrates) and hormone‐sensitive lipase (HSL); parallelly, inhibition of G0/G1 switch protein 2 (G0S2) and upregulation of adipose triglyceride lipase (ATGL) were observed (Figure 2D,E). The gene discussed is G0S2; the disease is neoplasm.