The unraveling of an unforeseen, selective vulnerability of silibinin-treated tumor cells to the hexosamine biosynthesis pathway inhibitor azaserine using genomically edited isogenic models might exemplify how to exploit the therapeutic usage of silibinin in combination with certain targetable weaknesses in specific subtypes of lung cancer (e.g., KRAS/STK11 co-mutant tumors with dependence on the hexosamine biosynthesis pathway through GFPT2 [104]). Here, STK11 is linked to neoplasm.